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Systemic sensory confusion?

Systemic sensory confusion?


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Sometimes when a person gets touched on one part of the body they feel it else where and may think it came from a different part of the body. What causes this? Other examples are similar to why you can trick your self into thinking your arms are heavier than they really are. another would be that you can close your eyes and move in circles up and down your arm slowly and then when you guess where u are touching your hand is higher or lower than expected. What causes these things?


The situations you describe involve what is called proprioception or the feedback to the brain of where your arms and limbs are in space. As APengioun mentioned, this is a complicated undertaking and if information is restricted, for example eyes are closed then the sense of where your limbs are gets messed up. As for your title, it's not really neuronal confusion as it is confusion of the sensory system if you can call it that. This includes sensory neurons from your limbs as well as central neurons in the brain that further process your information.


When our brain works out where a part of our body is in relation to another part of our body, or in relation to anything for that matter, we combine:

  • visual information
  • information about how much our muscles are contracted
  • how much our joints are contracted
  • different forces being applied on our arms/legs or other body parts
  • where it remembers we used to be
  • how much force we applied to move where we wanted to move
  • where we would therefore expect to be
  • and many other things

That's quite a few things that our body relies on! The one that's most fine tuned is our vision. Let's face it, whatever we are actively doing with our hands requires the most skill and knowledge of where our hands etc. are. It is also the system that we rely on the most. But other systems are helpful to make sure we don't fall, grabbing on to things and making sure we reflexively contract the opposite muscles to prevent falling, stop us dropping things and lot's more. It doesn't matter if they're not accurate, they just need to be fast and in doing so they can't be extremely exact.

When we don't use vision, we rely on these other things. They're made to quickly adapt (e.g. hold a shopping bag for a while and when you let go your arm feels light or when you get out of a swimming pool your body feels heavy) and it is important that they do this to allow their functions as listed in the last paragraph.


Systemic sensory confusion? - Biology

You Have Eight Sensory Systems

(Please note: figures below are from Wikipedia)

DESCRIPTION OF THE EIGHT SENSORY SYSTEMS

The five basic sensory systems:

The three sensory systems Ayres focused on in describing sensory integration dysfunction:

The most recently discussed set of sensations related to internal organs

A. The five basic sensory systems:

The visual system is responsible for seeing.

The primary visual area of the brain is the occipital lobe (see figure). Projections are received from the retina (through the thalamus) where different types of information are encoded. Types of visual information include: color, shape, orientation, and motion. From the ventral stream in the occipital lobe information projects to the temporal lobe to process what objects are. From the dorsal stream, information goes to the parietal lobes to process where objects are located.

The auditory system is responsible for hearing.

The primary auditory cortex is located in the superior temporal gyrus of the brain (see figure). Specific sound frequencies can be mapped precisely onto the primary auditory cortex. Particular areas in the auditory cortex process changes in sound frequency or amplitude, while other areas process combinations of sound frequencies. The major area involved in comprehending language, (called Wernike’s area) is located in the left hemisphere in most people.

The olfactory system is responsible for processing smell.

The olfactory bulb is located in the most forward part of the brain on the bottom side of the brain (see figure). The olfactory bulb transmits smell information from the nose to the brain, and is thus necessary for a proper sense of smell. Unlike the other sensory systems, the olfactory bulb has only one source of sensory input (neurons of the olfactory epithelium) and one output. Thus it is assumed to be more of a filter than an associative circuit that has many inputs and many outputs.

The olfactory bulb does receive “top-down” information from areas such as the amygdala, neocortex, hippocampus, and others. It has four functions:

  • discriminating among odors
  • enhancing detection of odors
  • filtering out many background odors
  • allowing higher brain areas related to arousal and attention to modify the detection and/or the discrimination of odors

Looking up from the base of the brain

The Gustatory system is responsible for the sense of taste.

It allows us to discriminate between safe and harmful foods. Usually, individuals prefer sweet and salty tastes to sour or bitter tastes. Detecting salt is critical to keeping a regulated and stable internal body environment. This taste is perceived positivity because it facilitates re-uptake of water into the blood. Since it helps survival, salt is perceived as a pleasant taste by most humans.

Sour taste can be good in small quantities, but when it gets too sour it becomes unpleasant to taste. This has occurred through evolution to protect us from eating over-ripe fruit, rotten meat, and other spoiled foods (dangerous because of bacteria which grow in these environments).

The bitter taste is almost completely unpleasant to humans. This is because many dangerous pharmacological agents taste bitter, including caffeine, nicotine, and strychnine. Some bitter tastes can be overcome (note how popular Starbucks is world wide! Also note how many medicines when chewed, have a bitter taste, apparently being interpreted by our bodies as poisons.)

Sweet taste signals that carbohydrates are present. Carbohydrates have a high calorie count and are desirable (humans in the distant past did not know when their next meal would occur, so they evolved to want/need to eat sweet tastes.)

The primary gustatory cortex is located near the somatotopic region for the tongue, in the insular cortex deep in the lateral fissure with the secondary taste areas in the opercula (see figure). This means the location is folded deeply within the cortex within the lateral sulcus between the temporal and frontal lobes.

The tactile system is responsible for processing touch information from the body.

The body sends tactile information to the somatosensory cortex through neural pathways to the spinal cord, the brain stem, and the thalamus. The primary somatosensory cortex is the primary receptive area for touch sensations and is located in the lateral postcentral gyrus, a prominent structure in the parietal lobe of the human brain.

Due to its many connections to other brain areas, the somatosensory cortex is the part of the nervous system that integrates touch, pressure, temperature, and pain.

The tactile system is extremely important in SPD. Many individuals with the disorder have tactile symptoms such as tactile defensiveness or under-responsivity to touch and pain. The touch system is one of the three foundational systems used in sensory integration treatment.

B. The three sensory systems Ayres focused on in describing the treatment of sensory integration dysfunction:

5. Tactile system (see description above)

The vestibular system contributes to balance and orientation in space. It is the leading system informing us about movement and position of head relative to gravity.

Our movements include two positions rotations and linear directionality. Thus, the vestibular system has two related components: the semicircular canal system, (related to detecting rotation) and the otoliths, (related to detecting linear acceleration/deceleration).

The vestibular system sends signals primarily to the neural parts of the brain that control our eye movements, and that keep us upright.

The vestibular system contains three semicircular canals, which are approximately at right angles to each other:

the horizontal canal, which detects rotation around a vertical axis (as when you do spins in ice skating),

the anterior semicircular canal, detects movement in forward/backward plane as in a nodding movement,

the posterior canal, detects movement in a frontal plane as in when cartwheeling.

The canal on each side has an almost parallel counterpart on the other side. Each pair of canals works in a push-pull fashion: when one is stimulated, its partner is inhibited. Together the partners allow us to sense rotation in all directions.

Emphasis on the function of the vestibular system comes from Ayres influence when she identified sensory processing disorders as a new condition. This sensory system has a broad influence in many parts of the brain projecting to:

  • The cerebellum (to effect movements of the head, eyes, and posture).
  • Cranial nerves III, IV, and VI (to permit the eyes to fix on a moving object while staying in focus).
  • Reticular formation (to signal how to adjust circulation and breathing when the body assumes a new position).
  • Spinal Cord (to allow quick reflex reactions related to balancing).
  • Thalamus (to control head and body motor responses).

The information above is only a simple introduction to the role of the vestibular system as it relates to SPD. The figure below depicts the complex vestibular system. This figure is in the public domain from Gray’s Anatomy (book).

Proprioception (sense of muscle and/or joint movements) System

The proprioceptive system (sometimes abbreviated as “prop” by therapists when they talk about it) senses the position, location, orientation, and movement of the body muscles and joints. Proprioception provides us with the sense of the relative position of neighboring parts of the body and effort used to move body parts.

Proprioception is activated by input to a proprioceptor in the periphery of the body. The proprioceptive sense combines sensory information from neurons in the inner ear (detecting motion and orientation) and stretch receptors in the muscles and the joint-supporting ligaments for stance.

Two types of proprioception exist:

  • Conscious proprioception, which travels up the posterior column-medial lemniscus pathway to the cerebrum and
  • Unconscious proprioception which travels up the dorsal spinocerebellar tract,[20] to the cerebellum.

Proprioception was felt by Ayres to be the foundation (with vestibular impairments) of SPD. It is one of the three sensory systems used by SI trained therapists as the cornerstone of the sensory aspect of advanced treatment.

Temporary proprioceptive impairment is reported during times of quick growth, mostly during adolescence. Other large increases or drops in bodyweight/size due to fluctuations of fat (e.g., liposuction) and/or muscle content (e.g., body-building) also affect proprioception.

Proprioception is occasionally impaired in typically developing individuals, for example, if you are tired. Generally speaking we do not notice out proprioceptive sense because we disregard through habituation, desensitization, or adaptation sensory stimuli that is continuously present. In essence, the habituation makes the proprioceptive sensory impressions disappear. One practical advantage of this is that unnoticed sensation continue in the background while an individual’s attention can move to another concern.

Temporary impairment of proprioception has also been known to occur from an overdose of vitamin B6 and or by cytotoxic factors such as chemotherapy.

The eighth, often neglected, but frequently problematic sensory system in SPD is the Interoceptive System. Interoception refers to sensations related to the physiological/physical condition of the body. Interoceptors are internal sensors that provide a sense of what our internal organs are feeling. Hunger and thirst are examples of interoception.

Interoception detects responses that guide regulation, including hunger, heart rate, respiration and elimination. The Interoceptive stimulation is detected through nerve endings lining the respiratory and digestive mucous membranes. Interoception works the vestibular and proprioceptive senses to determine how an individual perceives their own body. Well-modulated interoception helps the individual detect proprioceptive and vestibular sensation normally. For example, if a person feels his/her heart pounding, while it is not comfortable, trauma from the stimulation is not likely nor will the stimulation be craved. The same is true for hunger and thirst, as well as the feeling of the need to urinate or have a bowel movement.

Interoception is associated with autonomic motor control, and is different than mechano-reception (in the skin) and proprioception (in the muscles and joints). Interoception is located in the dorsal posterior insula and it creates distinct feelings from the body including pain, temperature, itch, muscular and visceral sensations, vasomotor activity, hunger, thirst, and the need for air. In humans, the primary interoceptive activity occurs in the right anterior insula, which provides the basis for subjective feelings of ones’ emotional awareness.

Some researchers believe that our perceptions of well-being, energy and stress are based on sensations representing the physiological condition of our bodies. They suggest that interoception is a foundation subjective feelings, emotion and self-awareness. There is evidence that the anterior insula-cingulate system may integrate Interoceptive information with emotional salience to form a subjective representation of the body while the mid-cingulate cortex, are more likely involved in environmental monitoring, response selection, and body orientation (see Taylor KS, Seminowicz DA, Davis KD (2009). Two systems of resting state connectivity between the insula and cingulate cortex. Human brain mapping, 30(9), 2731-2745).

See below for general diagram of the neuroanatomical locations noted in above descriptions. The brains depicted below are shown from a side view with the nose pointing to the left.


Reception

The first step in sensation is reception, which is the activation of sensory receptors by stimuli such as mechanical stimuli (being bent or squished, for example), chemicals, or temperature. The receptor can then respond to the stimuli. The region in space in which a given sensory receptor can respond to a stimulus, be it far away or in contact with the body, is that receptor’s receptive field. Think for a moment about the differences in receptive fields for the different senses. For the sense of touch, a stimulus must come into contact with body. For the sense of hearing, a stimulus can be a moderate distance away (some baleen whale sounds can propagate for many kilometers). For vision, a stimulus can be very far away for example, the visual system perceives light from stars at enormous distances.


Systemic sensory confusion? - Biology

The Sensory Nervous System

The Sensory Nervous System: Internal Senses
The Internal Senses include Proprioception and inputs responsible for regulating homeostasis. Homeostasis is a state or tendency towards equilibrium.

Proprioceptors: Proprioception: Sensors that keep track of where the body is in space. The sensory nervous system includes internal monitoring systems that allow us to coordinate movement.

  • Mechanoreceptors: Proprioception is carried out by Mechanoreceptors: In the joints, Pacinian Corpuscles detect deformation of the joints In the muscles, Muscle Spindles detect stretching of the muscle fibers In the muscles where tendons connect, Golgi Organs detect stretching of the tendons.
  • Vestibular system: An aspect of knowing where you are in space is knowing your orientation One component of your ears, the vestibular system informs your brain of how your body is oriented in space.

The Sensory Nervous System: External Senses
Sight: The retina is the neural portion of the eye Photons (light) activates receptors on the retina and the signal is transported to the CNS via the optic nerve.

  • Smell: Aromatic compounds are passed over the olfactory epithelium when you breathe. The olfactory epithelium contains nerve endings that signal to the olfactory bulb and other centers in the brain.
  • Touch: Skin: Three separate kinds of nerves detect sensations on the skin 1. Mechanoreceptors: Detect pressure and tension on the skin 2. Thermoreceptors: Detect the temperature of the stimulus 3. Nociceptors: Detect painful stimuli.
  • Hearing: Detect sounds and air pressure. Organ of Corti Sound in the form of pressure waves enter the ear, pass through the middle ear and vibrate a membrane in an elegant organ called the Organ of Corti.
  • Taste: Receptors on our tongue act in concert with the olfactory system to distinguish taste. There are five basic taste receptors: Salty, Sour, Bitter, Sweet and Umami.

This tutorial discusses the organization and integration of the sensory nervous system. The sensory nervous system receives information from the environment such as touch or heat, and relays this information back to the central nervous system for processing.

Specific Tutorial Features:

A detailed description of the five, major senses and how they function within the sensory nervous system is presented.
The connection between the sensory nervous system and its interactions with the central nervous system is illustrated.

  • Concept map showing inter-connections of new concepts in this tutorial and those previously introduced.
  • Definition slides introduce terms as they are needed.
  • Visual representation of concepts
  • Examples given throughout to illustrate how the concepts apply.
  • A concise summary is given at the conclusion of the tutorial.

The Sensory Nervous System: Internal Senses

The Sensory Nervous System: External Senses

See all 24 lessons in Anatomy and Physiology, including concept tutorials, problem drills and cheat sheets: Teach Yourself Anatomy and Physiology Visually in 24 Hours


Biology of Sensory Systems , Second Edition

Biology of Sensory Systems has thus been completely revised and takes a molecular, evolutionary and comparative approach, providing an overview of sensory systems in vertebrates, invertebrates and prokaryotes, with a strong focus on human senses.

Written by a renowned author with extensive teaching experience, the book covers, in six parts, the general features of sensory systems, the mechanosenses, the chemosenses, the senses which detect electromagnetic radiation, other sensory systems including pain, thermosensitivity and some of the minority senses and, finally, provides an outline and discussion of philosophical implications.

  • Greater emphasis on molecular biology and intracellular mechanisms
  • New chapter on genomics and sensory systems
  • Sections on TRP channels, synaptic transmission, evolution of nervous systems, arachnid mechanosensitive sensilla and photoreceptors, electroreception in the Monotremata, language and the FOXP2 gene, mirror neurons and the molecular biology of pain

Updated passages on human olfaction and gustation.

Over four hundred illustrations, boxes containing supplementary material and self-assessment questions and a full bibliography at the end of each part make Biology of Sensory Systems essential reading for undergraduate students of biology, zoology, animal physiology, neuroscience, anatomy and physiological psychology. The book is also suitable for postgraduate students in more specialised courses such as vision sciences, optometry, neurophysiology, neuropathology, developmental biology.

Praise from the reviews of the first edition:

"An excellent advanced undergraduate/postgraduate textbook." ASLIB BOOK GUIDE

"The emphasis on comparative biology and evolution is one of the distinguishing features of this self-contained book. . this is an informative and thought-provoking text. " TIMES HIGHER EDUCATIONAL SUPPLEMENT


Contents

Chronic stress and a lack of coping resources available or used by an individual can often lead to the development of psychological issues such as delusions, [7] depression and anxiety (see below for further information). [8] This is particularly true regarding chronic stressors. These are stressors that may not be as intense as an acute stressor like a natural disaster or a major accident, but they persist over longer periods of time. These types of stressors tend to have a more negative effect on health because they are sustained and thus require the body's physiological response to occur daily. [9]

This depletes the body's energy more quickly and usually occurs over long periods of time, especially when these microstressors cannot be avoided (i.e. stress of living in a dangerous neighborhood). See allostatic load for further discussion of the biological process by which chronic stress may affect the body. For example, studies have found that caregivers, particularly those of dementia patients, have higher levels of depression and slightly worse physical health than non-caregivers. [9]

When humans are under chronic stress, permanent changes in their physiological, emotional, and behavioral responses may occur. [10] Chronic stress can include events such as caring for a spouse with dementia, or may result from brief focal events that have long term effects, such as experiencing a sexual assault. Studies have also shown that psychological stress may directly contribute to the disproportionately high rates of coronary heart disease morbidity and mortality and its etiologic risk factors. Specifically, acute and chronic stress have been shown to raise serum lipids and are associated with clinical coronary events. [11]

However, it is possible for individuals to exhibit hardiness—a term referring to the ability to be both chronically stressed and healthy. [12] Even though psychological stress is often connected with illness or disease, most healthy individuals can still remain disease-free after being confronted with chronic stressful events. This suggests that there are individual differences in vulnerability to the potential pathogenic effects of stress individual differences in vulnerability arise due to both genetic and psychological factors. In addition, the age at which the stress is experienced can dictate its effect on health. Research suggests chronic stress at a young age can have lifelong effects on the biological, psychological, and behavioral responses to stress later in life. [13]

The term "stress" had none of its contemporary connotations before the 1920s. It is a form of the Middle English destresse, derived via Old French from the Latin stringere, "to draw tight". [14] The word had long been in use in physics to refer to the internal distribution of a force exerted on a material body, resulting in strain. In the 1920s and '30s, biological and psychological circles occasionally used the term to refer to a mental strain or to a harmful environmental agent that could cause illness.

Walter Cannon used it in 1926 to refer to external factors that disrupted what he called homeostasis. [15] But ". stress as an explanation of lived experience is absent from both lay and expert life narratives before the 1930s". [16] Physiological stress represents a wide range of physical responses that occur as a direct effect of a stressor causing an upset in the homeostasis of the body. Upon immediate disruption of either psychological or physical equilibrium the body responds by stimulating the nervous, endocrine, and immune systems. The reaction of these systems causes a number of physical changes that have both short- and long-term effects on the body. [ citation needed ]

The Holmes and Rahe stress scale was developed as a method of assessing the risk of disease from life changes. [17] The scale lists both positive and negative changes that elicit stress. These include things such as a major holiday or marriage, or death of a spouse and firing from a job.

Homeostasis is a concept central to the idea of stress. [18] In biology, most biochemical processes strive to maintain equilibrium (homeostasis), a steady state that exists more as an ideal and less as an achievable condition. Environmental factors, internal or external stimuli, continually disrupt homeostasis an organism's present condition is a state of constant flux moving about a homeostatic point that is that organism's optimal condition for living. [19] Factors causing an organism's condition to diverge too far from homeostasis can be experienced as stress. A life-threatening situation such as a major physical trauma or prolonged starvation can greatly disrupt homeostasis. On the other hand, an organism's attempt at restoring conditions back to or near homeostasis, often consuming energy and natural resources, can also be interpreted as stress. [20]

The ambiguity in defining this phenomenon was first recognized by Hans Selye (1907–1982) in 1926. In 1951 a commentator loosely summarized Selye's view of stress as something that ". in addition to being itself, was also the cause of itself, and the result of itself". [21] [22]

First to use the term in a biological context, Selye continued to define stress as "the non-specific response of the body to any demand placed upon it". Neuroscientists such as Bruce McEwen and Jaap Koolhaas believe that stress, based on years of empirical research, "should be restricted to conditions where an environmental demand exceeds the natural regulatory capacity of an organism". [23] Indeed, in 1995 Toates already defined stress as a "chronic state that arises only when defense mechanisms are either being chronically stretched or are actually failing," [24] while according to Ursin (1988) stress results from an inconsistency between expected events ("set value") and perceived events ("actual value") that cannot be resolved satisfactorily, [25] which also puts stress into the broader context of cognitive-consistency theory. [26]

Stress can have many profound effects on the human biological systems. [27] Biology primarily attempts to explain major concepts of stress using a stimulus-response paradigm, broadly comparable to how a psychobiological sensory system operates. The central nervous system (brain and spinal cord) plays a crucial role in the body's stress-related mechanisms. Whether one should interpret these mechanisms as the body's response to a stressor or embody the act of stress itself is part of the ambiguity in defining what exactly stress is.

The central nervous system works closely with the body's endocrine system to regulate these mechanisms. The sympathetic nervous system becomes primarily active during a stress response, regulating many of the body's physiological functions in ways that ought to make an organism more adaptive to its environment. Below there follows a brief biological background of neuroanatomy and neurochemistry and how they relate to stress. [ citation needed ]

Stress, either severe, acute stress or chronic low-grade stress may induce abnormalities in three principal regulatory systems in the body: serotonin systems, catecholamine systems, and the hypothalamic-pituitary-adrenocortical axis. Aggressive behavior has also been associated with abnormalities in these systems. [28]

The brain endocrine interactions are relevant in the translation of stress into physiological and psychological changes. The autonomic nervous system (ANS), as mentioned above, plays an important role in translating stress into a response. The ANS responds reflexively to both physical stressors (for example baroreception), and to higher level inputs from the brain. [29]

The ANS is composed of the parasympathetic nervous system and sympathetic nervous system, two branches that are both tonically active with opposing activities. The ANS directly innervates tissue through the postganglionic nerves, which is controlled by preganglionic neurons originating in the intermediolateral cell column. The ANS receives inputs from the medulla, hypothalamus, limbic system, prefrontal cortex, midbrain and monoamine nuclei. [30]

The activity of the sympathetic nervous system drives what is called the "fight or flight" response. The fight or flight response to emergency or stress involves mydriasis, increased heart rate and force contraction, vasoconstriction, bronchodilation, glycogenolysis, gluconeogenesis, lipolysis, sweating, decreased motility of the digestive system, secretion of the epinephrine and cortisol from the adrenal medulla, and relaxation of the bladder wall. The parasympathetic nervous response, "rest and digest", involves return to maintaining homeostasis, and involves miosis, bronchoconstriction, increased activity of the digestive system, and contraction of the bladder walls. [29] Complex relationships between protective and vulnerability factors on the effect of childhood home stress on psychological illness, cardiovascular illness and adaption have been observed. [31] ANS related mechanisms are thought to contribute to increased risk of cardiovascular disease after major stressful events. [32]

The HPA axis is a neuroendocrine system that mediates a stress response. Neurons in the hypothalamus, particularly the paraventricular nucleus, release vasopressin and corticotropin releasing hormone, which travel through the hypophysial portal vessel where they travel to and bind to the corticotropin-releasing hormone receptor on the anterior pituitary gland. Multiple CRH peptides have been identified, and receptors have been identified on multiple areas of the brain, including the amygdala. CRH is the main regulatory molecule of the release of ACTH. [33]

The secretion of ACTH into systemic circulation allows it to bind to and activate Melanocortin receptor, where it stimulates the release of steroid hormones. Steroid hormones bind to glucocorticoid receptors in the brain, providing negative feedback by reducing ACTH release. Some evidence supports a second long term feedback that is non-sensitive to cortisol secretion. The PVN of the hypothalamus receives inputs from the nucleus of the solitary tract, and lamina terminalis. Through these inputs, it receives and can respond to changes in blood. [33]

The PVN innervation from the brain stem nuclei, particularly the noradrenergic nuclei stimulate CRH release. Other regions of the hypothalamus both directly and indirectly inhibit HPA axis activity. Hypothalamic neurons involved in regulating energy balance also influence HPA axis activity through the release of neurotransmitters such as neuropeptide Y, which stimulates HPA axis activity. Generally, the amygdala stimulates, and the prefrontal cortex and hippocampus attenuate, HPA axis activity however, complex relationships do exist between the regions. [33]

The immune system may be heavily influenced by stress. The sympathetic nervous system innervates various immunological structures, such as bone marrow and the spleen, allowing for it to regulate immune function. The adrenergic substances released by the sympathetic nervous system can also bind to and influence various immunological cells, further providing a connection between the systems. The HPA axis ultimately results in the release of cortisol, which generally has immunosuppressive effects. However, the effect of stress on the immune system is disputed, and various models have been proposed in an attempt to account for both the supposedly "immunodeficiency" linked diseases and diseases involving hyper activation of the immune system. One model proposed to account for this suggests a push towards an imbalance of cellular immunity(Th1) and humoral immunity(Th2). The proposed imbalance involved hyperactivity of the Th2 system leading to some forms of immune hypersensitivity, while also increasing risk of some illnesses associated with decreased immune system function, such as infection and cancer. [6]

Chronic stress is a term sometimes used to differentiate it from acute stress. Definitions differ, and may be along the lines of continual activation of the stress response, [34] stress that causes an allostatic shift in bodily functions, [4] or just as "prolonged stress". [35] For example, results of one study demonstrated that individuals who reported relationship conflict lasting one month or longer have a greater risk of developing illness and show slower wound healing. Similarly, the effects that acute stressors have on the immune system may be increased when there is perceived stress and/or anxiety due to other events. For example, students who are taking exams show weaker immune responses if they also report stress due to daily hassles. [36] While responses to acute stressors typically do not impose a health burden on young, healthy individuals, chronic stress in older or unhealthy individuals may have long-term effects that are detrimental to health. [37]

Immunological Edit

Acute time-limited stressors, or stressors that lasted less than two hours, results in an up regulation of natural immunity and down regulation of specific immunity. This type of stress saw in increase in granulocytes, natural killer cells, IgA, Interleukin 6, and an increase in cell cytotoxicity. Brief naturalistic stressors elicit a shift from Th1(cellular) to Th2(humoral) immunity, while decreased T-cell proliferation, and natural killer cell cytotoxicity. Stressful event sequences did not elicit a consistent immune response however, some observations such as decreased T-Cell proliferation and cytotoxicity, increase or decrease in natural killer cell cytotoxicity, and an increase in mitogen PHA. Chronic stress elicited a shift toward Th2 immunity, as well as decreased interleukin 2, T cell proliferation, and antibody response to the influenza vaccine. Distant stressors did not consistently elicit a change in immune function. [6]

Infectious Edit

Some studies have observed increased risk of upper respiratory tract infection during chronic life stress. In patients with HIV, increased life stress and cortisol was associated with poorer progression of HIV. [34]

Chronic disease Edit

A link has been suggested between chronic stress and cardiovascular disease. [34] Stress appears to play a role in hypertension, and may further predispose people to other conditions associated with hypertension. [38] Stress may also precipitate a more serious, or relapse into abuse of alcohol. [4] Stress may also contribute to aging and chronic diseases in aging, such as depression and metabolic disorders. [39]

The immune system also plays a role in stress and the early stages of wound healing. It is responsible for preparing the tissue for repair and promoting recruitment of certain cells to the wound area. [36] Consistent with the fact that stress alters the production of cytokines, Graham et al. found that chronic stress associated with care giving for a person with Alzheimer's disease leads to delayed wound healing. Results indicated that biopsy wounds healed 25% more slowly in the chronically stressed group, or those caring for a person with Alzheimer's disease. [40]

Development Edit

Chronic stress has also been shown to impair developmental growth in children by lowering the pituitary gland's production of growth hormone, as in children associated with a home environment involving serious marital discord, alcoholism, or child abuse. [41]

More generally, prenatal life, infancy, childhood, and adolescence are critical periods in which the vulnerability to stressors is particularly high. [42] [43]

Psychopathology Edit

Chronic stress is seen to affect the parts of the brain where memories are processed through and stored. When people feel stressed, stress hormones get over-secreted, which affects the brain. This secretion is made up of glucocorticoids, including cortisol, which are steroid hormones that the adrenal gland releases, although this can increase storage of flashbulb memories it decreases long-term potentiation (LTP). [44] [45] The hippocampus is important in the brain for storing certain kinds of memories and damage to the hippocampus can cause trouble in storing new memories but old memories, memories stored before the damage, are not lost. [46] Also high cortisol levels can be tied to the deterioration of the hippocampus and decline of memory that many older adults start to experience with age. [45] These mechanisms and processes may therefore contribute to age-related disease, or originate risk for earlier-onset disorders. For instance, extreme stress (e.g. trauma) is a requisite factor to produce stress-related disorders such as post-traumatic stress disorder. [5]

Chronic stress also shifts learning, forming a preference for habit based learning, and decreased task flexibility and spatial working memory, probably through alterations of the dopaminergic systems. [30] Stress may also increase reward associated with food, leading to weight gain and further changes in eating habits. [47] Stress may contribute to various disorders, such as fibromyalgia, [48] chronic fatigue syndrome, [49] depression, [50] and functional somatic syndromes. [51]

Eustress Edit

Selye published in year 1975 a model dividing stress into eustress and distress. [52] Where stress enhances function (physical or mental, such as through strength training or challenging work), it may be considered eustress. Persistent stress that is not resolved through coping or adaptation, deemed distress, may lead to anxiety or withdrawal (depression) behavior.

The difference between experiences that result in eustress and those that result in distress is determined by the disparity between an experience (real or imagined) and personal expectations, and resources to cope with the stress. Alarming experiences, either real or imagined, can trigger a stress response. [53]

Coping Edit

Responses to stress include adaptation, psychological coping such as stress management, anxiety, and depression. Over the long term, distress can lead to diminished health and/or increased propensity to illness to avoid this, stress must be managed.

Stress management encompasses techniques intended to equip a person with effective coping mechanisms for dealing with psychological stress, with stress defined as a person's physiological response to an internal or external stimulus that triggers the fight-or-flight response. Stress management is effective when a person uses strategies to cope with or alter stressful situations.

There are several ways of coping with stress, [54] such as controlling the source of stress or learning to set limits and to say "no" to some of the demands that bosses or family members may make.

A person's capacity to tolerate the source of stress may be increased by thinking about another topic such as a hobby, listening to music, or spending time in a wilderness.

A way to control stress is first dealing with what is causing the stress if it is something the individual has control over. Other methods to control stress and reduce it can be: to not procrastinate and leave tasks for the last minute, do things you like, exercise, do breathing routines, go out with friends, and take a break. Having support from a loved one also helps a lot in reducing stress. [45]

One study showed that the power of having support from a loved one, or just having social support, lowered stress in individual subjects. Painful shocks were applied to married women's ankles. In some trials women were able to hold their husband's hand, in other trials they held a stranger's hand, and then held no one's hand. When the women were holding their husband's hand, the response was reduced in many brain areas. When holding the stranger's hand the response was reduced a little, but not as much as when they were holding their husband's hand. Social support helps reduce stress and even more so if the support is from a loved one. [45]

Cognitive appraisal Edit

Lazarus [55] argued that, in order for a psychosocial situation to be stressful, it must be appraised as such. He argued that cognitive processes of appraisal are central in determining whether a situation is potentially threatening, constitutes a harm/loss or a challenge, or is benign.

Both personal and environmental factors influence this primary appraisal, which then triggers the selection of coping processes. Problem-focused coping is directed at managing the problem, whereas emotion-focused coping processes are directed at managing the negative emotions. Secondary appraisal refers to the evaluation of the resources available to cope with the problem, and may alter the primary appraisal.

In other words, primary appraisal includes the perception of how stressful the problem is and the secondary appraisal of estimating whether one has more than or less than adequate resources to deal with the problem that affects the overall appraisal of stressfulness. Further, coping is flexible in that, in general, the individual examines the effectiveness of the coping on the situation if it is not having the desired effect, s/he will, in general, try different strategies. [56]

Health risk factors Edit

Both negative and positive stressors can lead to stress. The intensity and duration of stress changes depending on the circumstances and emotional condition of the person suffering from it (Arnold. E and Boggs. K. 2007). Some common categories and examples of stressors include:

  • Sensory input such as pain, bright light, noise, temperatures, or environmental issues such as a lack of control over environmental circumstances, such as food, air and/or water quality, housing, health, freedom, or mobility.
  • Social issues can also cause stress, such as struggles with conspecific or difficult individuals and social defeat, or relationship conflict, deception, or break ups, and major events such as birth and deaths, marriage, and divorce.
  • Life experiences such as poverty, unemployment, clinical depression, obsessive compulsive disorder, heavy drinking, [57] or insufficient sleep can also cause stress. Students and workers may face performance pressure stress from exams and project deadlines.
  • Adverse experiences during development (e.g. prenatal exposure to maternal stress, [58][59] poor attachment histories, [60]sexual abuse) [61] are thought to contribute to deficits in the maturity of an individual's stress response systems. One evaluation of the different stresses in people's lives is the Holmes and Rahe stress scale.

General adaptation syndrome Edit

Physiologists define stress as how the body reacts to a stressor - a stimulus, real or imagined, that causes stress. Acute stressors affect an organism in the short term chronic stressors over the longer term. The general adaptation syndrome (GAS), developed by Hans Selye, is a profile of how organisms respond to stress GAS is characterized by three phases: a nonspecific mobilization phase, which promotes sympathetic nervous system activity a resistance phase, during which the organism makes efforts to cope with the threat and an exhaustion phase, which occurs if the organism fails to overcome the threat and depletes its physiological resources. [62]

Stage 1 Edit

Alarm is the first stage, which is divided into two phases: the shock phase and the antishock phase. [63]

  • Shock phase: During this phase, the body can endure changes such as hypovolemia, hypoosmolarity, hyponatremia, hypochloremia, hypoglycemia—the stressor effect. This phase resembles Addison's disease. The organism's resistance to the stressor drops temporarily below the normal range and some level of shock (e.g. circulatory shock) may be experienced.
  • Antishock phase: When the threat or stressor is identified or realized, the body starts to respond and is in a state of alarm. During this stage, the locus coeruleus and sympathetic nervous system activate the production of catecholamines including adrenaline, engaging the popularly-known fight-or-flight response. Adrenaline temporarily provides increased muscular tonus, increased blood pressure due to peripheral vasoconstriction and tachycardia, and increased glucose in blood. There is also some activation of the HPA axis, producing glucocorticoids (cortisol, aka the S-hormone or stress-hormone).

Stage 2 Edit

Resistance is the second stage. During this stage, increased secretion of glucocorticoids intensifies the body's systemic response. Glucocorticoids can increase the concentration of glucose, fat, and amino acid in blood. In high doses, one glucocorticoid, cortisol, begins to act similarly to a mineralocorticoid (aldosterone) and brings the body to a state similar to hyperaldosteronism. If the stressor persists, it becomes necessary to attempt some means of coping with the stress. The body attempts to respond to stressful stimuli, but after prolonged activation, the body's chemical resources will be gradually depleted, leading to the final stage.

Stage 3 Edit

The third stage could be either exhaustion or recovery:

  • Recovery stage follows when the system's compensation mechanisms have successfully overcome the stressor effect (or have completely eliminated the factor which caused the stress). The high glucose, fat and amino acid levels in blood prove useful for anabolic reactions, restoration of homeostasis and regeneration of cells.
  • Exhaustion is the alternative third stage in the GAS model. At this point, all of the body's resources are eventually depleted and the body is unable to maintain normal function. The initial autonomic nervous system symptoms may reappear (sweating, raised heart rate, etc.). If stage three is extended, long-term damage may result (prolonged vasoconstriction results in ischemia which in turn leads to cell necrosis), as the body's immune system becomes exhausted, and bodily functions become impaired, resulting in decompensation.

The result can manifest itself in obvious illnesses, such as general trouble with the digestive system (e.g. occult bleeding, melena, constipation/obstipation), diabetes, or even cardiovascular problems (angina pectoris), along with clinical depression and other mental illnesses. [ citation needed ]

The current usage of the word stress arose out of Hans Selye's 1930s experiments. He started to use the term to refer not just to the agent but to the state of the organism as it responded and adapted to the environment. His theories of a universal non-specific stress response attracted great interest and contention in academic physiology and he undertook extensive research programs and publication efforts. [64]

While the work attracted continued support from advocates of psychosomatic medicine, many in experimental physiology concluded that his concepts were too vague and unmeasurable. During the 1950s, Selye turned away from the laboratory to promote his concept through popular books and lecture tours. He wrote for both non-academic physicians and, in an international bestseller entitled Stress of Life, for the general public.

A broad biopsychosocial concept of stress and adaptation offered the promise of helping everyone achieve health and happiness by successfully responding to changing global challenges and the problems of modern civilization. Selye coined the term "eustress" for positive stress, by contrast to distress. He argued that all people have a natural urge and need to work for their own benefit, a message that found favor with industrialists and governments. [64] He also coined the term stressor to refer to the causative event or stimulus, as opposed to the resulting state of stress.

Selye was in contact with the tobacco industry from 1958 and they were undeclared allies in litigation and the promotion of the concept of stress, clouding the link between smoking and cancer, and portraying smoking as a "diversion", or in Selye's concept a "deviation", from environmental stress. [65]

From the late 1960s, academic psychologists started to adopt Selye's concept they sought to quantify "life stress" by scoring "significant life events", and a large amount of research was undertaken to examine links between stress and disease of all kinds. By the late 1970s, stress had become the medical area of greatest concern to the general population, and more basic research was called for to better address the issue. There was also renewed laboratory research into the neuroendocrine, molecular, and immunological bases of stress, conceived as a useful heuristic not necessarily tied to Selye's original hypotheses. The US military became a key center of stress research, attempting to understand and reduce combat neurosis and psychiatric casualties. [64]

The psychiatric diagnosis post-traumatic stress disorder (PTSD) was coined in the mid-1970s, in part through the efforts of anti-Vietnam War activists and the Vietnam Veterans Against the War, and Chaim F. Shatan. The condition was added to the Diagnostic and Statistical Manual of Mental Disorders as posttraumatic stress disorder in 1980. [66] PTSD was considered a severe and ongoing emotional reaction to an extreme psychological trauma, and as such often associated with soldiers, police officers, and other emergency personnel. The stressor may involve threat to life (or viewing the actual death of someone else), serious physical injury, or threat to physical or psychological integrity. In some cases, it can also be from profound psychological and emotional trauma, apart from any actual physical harm or threat. Often, however, the two are combined.

By the 1990s, "stress" had become an integral part of modern scientific understanding in all areas of physiology and human functioning, and one of the great metaphors of Western life. Focus grew on stress in certain settings, such as workplace stress, and stress management techniques were developed. The term also became a euphemism, a way of referring to problems and eliciting sympathy without being explicitly confessional, just "stressed out". It came to cover a huge range of phenomena from mild irritation to the kind of severe problems that might result in a real breakdown of health. In popular usage, almost any event or situation between these extremes could be described as stressful. [14] [64]

The American Psychological Association's 2015 Stress In America Study [67] found that nationwide stress is on the rise and that the three leading sources of stress were "money", "family responsibility", and "work".


A physiologist's view of homeostasis

Homeostasis is a core concept necessary for understanding the many regulatory mechanisms in physiology. Claude Bernard originally proposed the concept of the constancy of the “milieu interieur,” but his discussion was rather abstract. Walter Cannon introduced the term “homeostasis” and expanded Bernard's notion of 𠇌onstancy” of the internal environment in an explicit and concrete way. In the 1960s, homeostatic regulatory mechanisms in physiology began to be described as discrete processes following the application of engineering control system analysis to physiological systems. Unfortunately, many undergraduate texts continue to highlight abstract aspects of the concept rather than emphasizing a general model that can be specifically and comprehensively applied to all homeostatic mechanisms. As a result, students and instructors alike often fail to develop a clear, concise model with which to think about such systems. In this article, we present a standard model for homeostatic mechanisms to be used at the undergraduate level. We discuss common sources of confusion (“sticky points”) that arise from inconsistencies in vocabulary and illustrations found in popular undergraduate texts. Finally, we propose a simplified model and vocabulary set for helping undergraduate students build effective mental models of homeostatic regulation in physiological systems.

in 2007, a group of 21 biologists from a wide range of disciplines agreed that “homeostasis” was one of eight core concepts in biology (14). Two years later, the American Association of Medical Colleges and Howard Hughes Medical Institute in its report (1) on the scientific foundations for future physicians similarly identified the ability to apply knowledge about “homeostasis” as one of the core competencies (competency M1).

From our perspective as physiologists, it is clear that homeostasis is a core concept of our discipline. When we asked physiology instructors from a broad range of educational institutions what they thought the 𠇋ig ideas” (concepts) of physiology were, we found that they too identified “homeostasis” and �ll membranes” as the two most important big ideas in physiology (15). In a subsequent survey (16), physiology instructors ranked homeostasis as one of the core concepts critical to understanding physiology.

If, as these surveys indicate, the concept of homeostasis is central to understanding physiological mechanisms, one would expect that instructors and textbooks would present a consistent model of the concept. However, an examination of 11 commonly used undergraduate physiology and biology textbooks revealed that this is not necessarily the case (17). Explanations of the concept of homeostasis and subsequent references to the concept suffer from a number of shortcomings. Although these texts define some terms related to homeostatic regulatory systems, many authors do not use these terms consistently. Moreover, they do not always use consistent visual representations of the concept. In addition, the explanation of the concept often conflicts with the current understanding of homeostatic regulatory mechanisms. These limitations of textbooks most likely carry over to classroom instruction, thereby weakening the power of the concept as a unifying idea for understanding physiology.

The goals of this article are to develop a correct description and visual representation of a general homeostatic mechanism that can serve as a learning tool for faculty members and students. We will limit our discussion to homeostatic mechanisms found in organismal systems that maintain a constant extracellular compartment and will not consider other types of homeostasis. Although this tool can be useful at any academic level, our primary focus is its application at the undergraduate level when students are first introduced to the concept. We will also briefly discuss the history of the concept and then address the “sticky points” that may lead to confusion for faculty members and students alike when attempting to apply the concept to mammalian, organismal physiology. We conclude with suggestions for improving instruction on homeostasis and its applications.

History of the Concept of Homeostasis

Claude Bernard asserted that complex organisms are able to maintain their internal environment [extracellular fluid (ECF)] fairly constant in the face of challenges from the external world (8). He went on to say that 𠇊 free and independent existence is possible only because of the stability of the internal milieu” (3). Walter Cannon coined the term “homeostasis” with the intent of providing a term that would convey the general idea proposed some 50 yr earlier by Bernard (8). Cannon's view focused on maintaining a steady state within an organism regardless of whether the mechanisms involved were passive (e.g., water movement between capillaries and the interstitium reflecting a balance between hydrostatic and osmotic forces) or active (e.g., storage and release of intracellular glucose) (6). While we recognize the validity of both passive and active mechanisms of homeostasis, our consideration will focus exclusively on the active regulatory processes involved in maintaining homeostasis.

Early physiology textbooks reflected this broad definition by briefly mentioning Bernard's concept of the constancy of the internal milieu, but the term “homeostasis” was not used in discussions of specific regulatory mechanisms (9, 11, 4).

This situation began to change in the mid-1960s, when a branch of biomedical engineering emerged that focused on applying engineering control systems analysis to physiological systems (18, 19, 2, 20). Arthur Guyton was the first major physiology textbook author to include a control systems theory approach in his textbook, and his book included detailed attention to the body's many regulatory mechanisms (10). Hence, Guyton introduced many students to the concept of homeostasis as an active regulatory mechanism that tended to minimize disturbances to the internal environment.

Engineering control systems theory describes a variety of other mechanisms to maintain the stability of a system. Although many of these mechanisms may be found in biological systems (7), not all of them are components of homeostatic mechanisms. For instance, the ballistic system used by the nervous system for throwing a ball simply calculates in advance the pattern of commands needed to achieve some particular outcome based on previous experience (7). Here, there is no element involved that regulates the internal environment.

Homeostatic mechanisms originated to keep a regulated variable in the internal environment within a range of values compatible with life and, as has been more recently suggested, to reduce noise during information transfer in physiological systems (22). To emphasize the stabilizing process, we distinguish between a “regulated (sensed) variable” and a “nonregulated (controlled) variable” (5, 23). A regulated (sensed) variable is one for which a sensor exists within the system and that is kept within a limited range by physiological mechanisms (5). For example, blood pressure and body temperature are sensed variables. Baroreceptors and thermoreceptors exist within the system and provide the value of the pressure or temperature to the regulatory mechanism. We call variables that can be changed by the system, but for which sensors do not exist within the system, nonregulated (controlled) variables. Nonregulated variables are manipulated or modulated to achieve regulation of the variable being held constant. For example, heart rate can be changed by the autonomic nervous system to regulate blood pressure, but there are no sensors in the system that measure heart rate directly. Hence, heart rate is a nonregulated variable.

A simple model illustrating the fundamental engineering control system concepts relevant to homeostatic regulatory mechanisms is shown in Fig. 1 .

Diagram of a generic homeostatic regulatory system. If the value of the regulated variable is disturbed, this system functions to restore it toward its set point value and, hence, is also referred to as a negative feedback system.

This model, some version of which appears in many current physiology texts, includes the following five critical components that a regulatory system must contain to maintain homeostasis:

1. It must contain a sensor that measures the value of the regulated variable.

2. It must contain a mechanism for establishing the “normal range” of values for the regulated variable. In the model shown in Fig. 1 , this mechanism is represented by the “set point,” although this term is not meant to imply that this normal range is actually a “point” or that it has a fixed value. In the next section, we further discuss the notion of a set point.

3. It must contain an 𠇎rror detector” that compares the signal being transmitted by the sensor (representing the actual value of the regulated variable) with the set point. The result of this comparison is an error signal that is interpreted by the controller.

4. The controller interprets the error signal and determines the value of the outputs of the effectors.

5. The effectors are those elements that determine the value of the regulated variable.

Such a system operates in way that causes any change to the regulated variable, a disturbance, to be countered by a change in the effector output to restore the regulated variable toward its set point value. Systems that behave in this way are said to be negative feedback systems.

While the model shown in Fig. 1 is a relatively simple one, there is a great deal of information that can be packed into each of the boxes that constitute the model. Homeostasis can also be described as a hierarchically arranged set of statements, a conceptual framework, that contains whatever breath and depth of information is appropriate for a particular set of students in a course. We have developed and described such an “unpacking” of the core concept of homeostasis (12, 13). The model and the conceptual framework provide students with different tools for thinking about homeostasis.

Topics That Cause Confusion for Students and Instructors: Sticky Points

A sticky point is any conceptual difficulty that makes one's mental model of any phenomenon inaccurate and, hence, less useful. There are a number of factors that contribute to the generation of sticky points for both instructors and students:

The phenomenon in question is a complex one.

There are aspects of the phenomenon that are counterintuitive.

The language or terminology used to describe the phenomenon or concept is inconsistent.

The discipline's understanding of the phenomenon is uncertain or incomplete.

In this section, we will describe some sticky points about homeostatic regulatory mechanisms that we have uncovered as we have interacted with instructors and students about their understanding of homeostasis. We will address these sticky points in the form of a series of questions and answers.

What environment is regulated by organismal homeostasis?

Organismal homeostasis, as originally defined by Cannon (6), refers to physiological mechanisms that maintain relatively constant the variables related to the internal milieu of the organism. This includes variables related to the entire ECF compartment or to its subcompartments (e.g., the plasma). We will not be discussing intracellular homeostatic mechanisms.

Are all negative feedback systems homeostatic?

Although negative feedback is an essential element of homeostatic regulatory mechanisms, the presence of negative feedback in a system does not mean that the system is homeostatic in function. Negative feedback exists in many systems that do not involve homeostatic regulation. For example, negative feedback plays a role in the muscle stretch reflex, but this reflex is not involved with maintaining the constancy of the internal environment. In other cases, the presence of negative feedback may minimize oscillation of a variable, even though that variable itself is not maintained relatively constant (i.e., it is not a regulated variable). Control of the blood levels of cortisol is an example of the oscillating damping effects of negative feedback (see further discussion below).

Can other types of control mechanisms (e.g., feedforward) maintain homeostasis?

Feedforward or anticipatory control mechanisms permit the body to predict a change in the physiology of the organism and initiate a response that can reduce the movement of a regulated variable out of its normal range (7, 23). Thus, feedforward mechanisms may help minimize the effects of a perturbation and can help maintain homeostasis. For example, anticipatory increases in breathing frequency will reduce the time course of the response to exercise-induced hypoxia. Because of this, attempts have been made to broaden the definition of homeostasis to include a range of anticipatory mechanisms (23).

However, we have decided to limit our generic model of a homeostatic regulatory system ( Fig. 1 ) to one that illustrates negative feedback and demonstrates the minimization of an error signal. We have done this because our model is intended to help faculty members teach and students learn the core concept of homeostasis in introductory physiology (12, 13). There are additional complex features found in feedback systems that are not included here because our intention is to first help students make sense of the foundational concept of homeostatic regulation. As situations are encountered where this basic model is no longer adequate to predict system behavior (7, 23), additional elements like feedforward mechanisms can be added to the model.

What is a set point?

Understanding the concept of a set point is central to understanding the function of a homeostatic mechanism. The set point in an engineering control system is easily defined and understood it is the value of the regulated variable that the designer or operator of the system wants as the output of the system. The cruise control mechanism in an automobile is an example of a system with an easy to understand set point. The driver determines the desired speed for the car (the set point). The regulatory mechanism uses available effectors (the throttle actuators) and a negative feedback system to hold the speed constant in the face of changes in terrain and wind conditions. In such a system, we can envision an electronic circuit located in the engine control module that compares the actual ground speed with the set speed programmed by the driver and uses the error signal to control the throttle actuator appropriately.

In physiological systems, the set point is conceptually similar. However, one source of difficulty is that, in most cases, we do not know the molecular or cellular mechanisms that generate a signal of a particular magnitude. What is clear is that certain physiological systems behave as though there is a set point signal that is used to regulate a physiological variable (23).

Another challenge to our understanding of set points arises from the fact that set points are clearly changeable, either physiologically or as the result of a pathological change in the system (23). The mechanisms that cause variations in a set point can operate temporarily, permanently, or cyclically. Physiologically, this can occur as a result of discrete physiological phenomena (e.g., fever), the operation of hierarchical homeostats (e.g., regulation of ECF P co 2) (see Ref. 7), or through the influence of biological clocks (e.g., circadian or diurnal rhythms of body temperature). The observation that set points can be changed adds complexity to our understanding of homeostatic regulation and can lead to confusion about whether the measured change in a regulated variable results from a change in the physiological stimulus or from a changing set point (23). In these cases, it is important to make such distinctions between a change in the stimulus and the modulation of the set point to arrive at an accurate picture of how a particular homeostatically regulated system operates.

Do homeostatic mechanisms operate like an on/off switch?

Control signals are ALWAYS present, and they continuously determine the output of the effectors. Changes in the control signals alter effector outputs and therefore change the regulated variable. The amplitude of these control signals vary when there is an error signal (i.e., when the regulated variable is not the same as the set point). Thus, homeostatic regulation is a constant, continuous process and does not ordinarily operate as an on/off switch that results in an all-or-none response.

What is the difference between an effector and a physiological response?

Textbook diagrams and narratives can blur the distinction between the effector and a response generated by the effector, making it difficult for students to build a correct mental model. This problem can occur if, when a visual representation of a homeostatic mechanism is presented (see Fig. 1 ), a physiological response is placed in the same 𠇌oncept” box as the effector. For example, “increased secretion by sweat glands” and “vasodilation of blood vessels in the skin” might be identified as effectors in the control system for thermoregulation. However, only “sweat glands” and 𠇋lood vessels” are effectors, whereas “increased secretion” and “vasodilation” are the responses of the effectors. Comprehensive understanding of homeostatic mechanisms requires that we, and students, make clear distinctions between effectors and responses. The term �tor” should only be applied to a physical entity such as a cell, tissue, or organ, whereas responses such as secretion and vasodilation are actions, not physical entities.

Students may also be confused if only the change in the regulated variable is thought of as being the response of the effector. The change in the regulated variable is typically a consequence of changes in function caused by effectors that determine the value of the regulated variable. By applying the term “response” to only the change in the regulated variable, the intermediary steps between the action of the effector and the change in the regulated variable are not acknowledged explicitly. Under these circumstances, it would reasonable for students to conclude that the intermediary steps are, in some way, aspects of the effector rather than the effect of actions of the effectors. This practice may also reflect a lack of understanding of the difference between the regulated variable, e.g., body temperature, and all of the nonregulated variables that are modified (e.g., arteriole diameter and rate of sweat production) in the steps between the action of the effector and the change in the regulated variable.

What does “relatively constant over time” mean?

In the above sections, we emphasized that homeostatic mechanisms operate to keep a regulated variable in the internal environment “relatively constant.” This is a common phrase used to describe what normally happens to the value of the regulated variable over time. A potential sticky point arises from the use of this phrase. How much change can occur to a regulated variable that is held relatively constant? Three points of clarification need to be made. By saying relatively constant, we mean that:

1. Regulated variables are held within a narrower range of values than if they were not regulated.

2. The regulated value is maintained within a range that is consistent with the viability of the organism.

3. There are differences in the range of values permitted for different regulated variables.

The second point is key to understanding the range over which regulated variables can change homeostatic mechanisms operate to prevent a potentially lethal change in the internal environment. Indeed, as it is often used, relatively constant essentially serves as a surrogate phrase for within the range compatible with an organism's viability. For some regulated variables, the range is quite narrow (e.g., extracellular H + concentration or extracellular osmolarity). For other variables, the range can be broad under some circumstances (e.g., blood glucose concentration during the fed state) and narrow in other situations (e.g., blood glucose during the fasting state). The factors that contribute to the normal range or, in our model, the set point, of a particular variable are undoubtedly complex and, in most cases, have not been elucidated.

What physiological variables are homeostatically regulated?

To identify specific variables that may be homeostatically regulated, the five critical components illustrated in the model shown in Fig. 1 must be present. That is, a regulatory system for that variable must exist that contains the five critical components described in Fig. 1 . Based on this test, we have generated a partial list of the physiological variables that are homeostatically regulated ( Table 1 ). The list of widely recognized and clearly established regulated variables in humans includes a number of inorganic ions (e.g., H + , Ca 2+ , K + , and Na + ), blood-borne nutrients (e.g., glucose), blood pressure, blood volume, blood osmolarity, and core body temperature.

Table 1.

Homeostatically regulated variables typically found in undergraduate human physiology textbooks

Regulated VariableNormal Range or ValueSensor (Location If Known)Control Center (Location)EffectorsEffector Response
Arterial P o 275� mmHgChemosensors (carotid bodies and aortic body)Brain stemDiaphragm and respiratory musclesChange breathing frequency and tidal volume
Arterial P co 234� mmHgChemosensors (carotid bodies, aortic body, and the medulla)Brain stemDiaphragm and respiratory musclesChange breathing frequency and tidal volume
K + concentration3.5𠄵.0 meq/lChemosensors (adrenal cortex)Adrenal cortexKidneysAlter reabsorption/secretion of K +
Ca 2+ concentration4.3𠄵.3 meq/l (ionized)Chemosensors (parathyroid gland)Parathyroid glandBone, kidney, and intestineAlter reabsorption of Ca 2+ , alter resorption/building of bone, and alter absorption of Ca 2+
H + concentration (pH)35� nM (pH 7.35𠄷.45)Chemosensors (carotid bodies, aortic body, and floor of the fourth ventricle)Brain stemDiaphragm and respiratory musclesChange breathing frequency and tidal volume and change secretion/reabsorption of H + /bicarbonate ions
Chemosensors (kidney)KidneyKidney
Blood glucose concentration70� mg/dlFed state: chemosensors (pancreas)PancreasLiver, adipose tissue, and skeletal muscleAlter storage/metabolism/release of glucose and its related compounds
Fasting state: chemosensors (hypothalamus, pancreas)Hypothalamus
Core body temperature98.6ଏThermosensors (hypothalamus, skin)HypothalamusBlood vessels and sweat glands in the skin as well as skeletal musclesChange peripheral resistance, rate of sweat secretion rate, and shivering
Alter heat gains/losses
Mean arterial pressure93 mmHgMechanosensors (carotid sinus and aortic arch)MedullaHeart and blood vesselsAlter heart rate, peripheral resistance, inotropic state of the heart, and venomotor tone
Blood volume (effective circulating volume)5 litersMechanosensorsMedullaHeartAlter heart rate, peripheral resistance, and inotropic state of the heart
(Blood vessels: carotid bodies)HypothalamusBlood vesselsAlter Na + and water reabsorption
(Heart: atria and ventricle)AtriaKidneysAlter water absorption
(Kidney: juxtaglomerular apparatus and renal afferent arterioles)KidneyIntestine
Blood osmolality280� mosM/kgOsmosensors (hypothalamus)HypothalamusKidneysAlter water reabsorption

This table includes commonly found components of control systems involved in physiological regulation (i.e., homeostasis). This is not meant to be an exhaustive list but rather reflect the current understanding of homeostatically regulated variables that undergraduate physiology students should understand and be able to apply to problems (e.g., making predictions about responses to perturbations or explaining symptoms of disease).

A potential sticky point occurs when textbooks identify variables as homeostatically regulated even though the system involved does not have all of the required components. The proposition that certain metabolic waste products (e.g., nitrogenous wastes, bilirubin, and creatinine) are homeostatically regulated illustrates such a failure. We are not suggesting that the levels of these substances are not kept relatively constant by steady-state processes in the body. Rather, the concentrations of these substances are not maintained by a system that meets the definition of a homeostatic mechanism listed above. The body does not possess a physiological sensor for detecting these substances in the ECF and therefore cannot homeostatically regulate the ECF concentration of these substances.

Conversely, some mechanisms for controlling the level of a physiological variable include one component of the model (e.g., negative feedback) and may give the appearance of homeostatic regulation but, in the final analysis, do not meet all criteria and should not be considered homeostatic. For example, textbook diagrams illustrating control of blood cortisol levels show several negative feedback loops. This can cause students to think that cortisol is a regulated variable. However, the sensed variable(s) in this system is(are) the variables (e.g., blood glucose or “stress”) whose values are processed by the higher brain centers or hypothalamus and result in the release of corticotropin-releasing hormone. The result of the negative feedback loops involving adrenocorticotropic hormone and cortisol is a modulation of the release rate of the respective hormones. Therefore, corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol should not be considered homeostatically regulated variables. They are signaling elements controlling the effectors that determine the value of the regulated variable(s).

Another possible source of confusion about the identification of regulated variables arises when a physiological variable is regulated under one set of circumstances but behaves as a controlled variable under other circumstances. This can happen if a regulated variable is under the control of two different homeostatic systems or if a regulated variable can be 𠇌oopted” by another homeostatic system. This often happens if a physiological variable plays a role in more than one function in the body.

It is here that the concept of nested homeostasis or hierarchies of homeostats can be helpful. Carpenter (7) has pointed out that there are circumstances in which the maintenance of one regulated variable at its set point value is more important for continued viability of the organism than the simultaneous regulation of another variable.

One example of this is provided by the value of P co 2 in the ECF. As a variable in the internal environment that affects cell viability, P co 2 meets all of the criteria for a homeostatically regulated variable. P co 2 in the ECF depends on the action of respiratory muscles that alter the rate and depth of ventilation. As such, P co 2 in the ECF is maintained within defined limits by a regulatory system that senses P co 2 and operates by negative feedback. However, as any student of acid-base physiology knows, P co 2 in the ECF is not maintained relatively constant during compensatory adjustments in the acid-base balance of the body. From the perspective of H + homeostasis, P co 2 functions as a controlled variable.

At this point, some of our students might ask “Which is it? Is P co 2 a regulated variable or is it a controlled variable?” Our answer is that P co 2 is 𠇋oth,” and we can explain this using the idea of nested homeostatic mechanisms. There are circumstance in which it is more important to maintain arterial H + concentration (pH) in the normal range that maintaining a constant P co 2, perhaps because of the particular impact of the H + concentration on cell survival. Therefore, effective regulation of the H + concentration of the ECF can only be achieved by allowing P co 2 to dramatically vary from its normal range during acid-base disturbances. By introducing the concept of nested homeostatic mechanisms, we have refined how we view P co 2 as a homeostatically regulated variable, and we have offered another way to resolve other, “sticky” situations where the authenticity of a homeostatically regulated variable might be called into question.

Best Practices in Teaching Homeostasis

Given the centrality of the concept of homeostasis (15, 16), one would expect that both instructional resources and instructors would provide a consistent model of the concept and apply this model to appropriate systems in which variables are sensed and maintained relatively constant.

However, examination of undergraduate textbooks revealed that this is not the case (17). The problems found include, but were not limited to, inconsistent language used to describe the phenomenon and incomplete or inadequate pictorial representations of the model. In addition, texts often define homeostasis early in the narrative but fail to reinforce application of the model when specific regulatory mechanisms are discussed (17).

Furthermore, our work focusing on developing a concept inventory for homeostatic regulation (12, 13) revealed considerable confusion among faculty members regarding the concept. We think this confusion may stem, in part, from the level of faculty uncertainty about the concept and degree of complexity of homeostatic regulatory mechanisms. Our discussion of the sticky points associated with homeostasis is an attempt to suggest potential sources of this confusion and to indicate ways that instructors can work through these difficulties.

How do we ameliorate this situation? We propose five strategies that will help in approaching the problem.

1. Faculty members members should adopt a standard set of terms associated with the model. There is inconsistency within and among textbooks with respect to the names for critical components of the model. We propose the terminology shown in Table 2 to be used when discussing homeostatic regulatory mechanisms.

Table 2.

Definitions of terms for homeostasis paper

Term
Control center (or integrator)The control center consists of an error detector and controller. It receives signals (information) from sensors, compares information (value of regulated variable) with the set point, integrates information from all sensors, and sends output signals (sends instructions or commands) to increase or decrease the activity of effectors. The control center determines and initiates the appropriate physiological response to any change or disturbance of the internal environment
ControllerThe component of the control center that receives signals (information) from the error detector and sends output signals (instructions or commands) to increase or decrease the activity of effectors. The controller initiates the appropriate physiological response to an error signal resulting from a change or disturbance of the regulated (sensed) variable.
EffectorA component whose activity or action contributes to determining the value of any variable the system. In this model, the effectors determine the value of the regulated (sensed) variable.
Error detectorThe component in the control center that determines (calculates) the difference between the set point value and the actual value of the regulated (sensed) variable. The error detector generates the error signal that is used to determine the output of the control center.
Error signalA signal that represents the difference between the set point value and the actual value of the regulated variable. The error signal is one of the input signals to the controller.
External environmentThe world outside of the body and its “state.” The state or conditions in the outside world can determine the state of many internal properties of the organism.
IntegratorThis is another term for the control center. The integrator processes information from the sensor and those components that determine the set point, determines any error signal present, and sends output signals (instructions or commands) to increase or decrease the activity of effectors.
Internal environmentThe internal environment is the extracellular fluid compartment. This is the environment in which the body's cells live. It is what Bernard meant by the “internal milieu.”
HomeostasisThe maintenance of a relatively stable internal environment by an organism in the face of a changing external environment and varying internal activity using negative feedback mechanisms to minimize an error signal.
Negative feedbackA control mechanism where the action of the effector (response) opposes a change in the regulated variable and returns it back toward the set point value.
Nonregulated variable (controlled variable)A variable whose value changes in response to effector activity but whose value is not directly sensed by the system. Controlled variables contribute to determination of the regulated variable. For example, heart rate and stroke volume (controlled variables) contribute to determining cardiac output (another controlled variable) that contributes to arterial blood pressure (a regulated variable).
Perturbation (disturbance)Any change in the internal or external environment that causes a change to a homeostatically regulated variable. Physiologically induced changes in the set point would not be considered a perturbation.
Regulated variable (sensed variable)Any variable for which sensors are present in the system and the value of which is kept within limits by a negative feedback system in the face of perturbations in the system. A regulated variable is any property or condition of the extracellular fluid that is kept relatively constant in the internal environment in order to ensure the viability (survival) of the organism.
ResponseThe change in the function or action of an effector.
Sensor (Receptor)A �vice” that measures the magnitude of some variable by generating an output signal (neural or hormonal) that is proportional to the magnitude of the stimulus. A sensor is a measuring �vice.” For some regulated variables, sensors are specialized sensory cells or “sensory receptors,” e.g., thermoreceptors, baroreceptors, or osmoreceptors. For other regulated variables, sensors are cellular components, e.g., the Ca 2+ -sensing receptor (a G protein-coupled receptor that senses blood Ca 2+ in the parathyroid gland).
Set pointThe range of values (range of magnitudes) of the regulated variable that the system attempts to maintain. Set point refers to the �sired value.” The set point is generally not a single value it is a range of values.

A glossary of terms used in discussing the core concept of homeostasis. The components of a homeostatically regulated system ( Fig. 1 ) are defined here as are some other terms that occur in teaching this concept.

2. A standard standard pictorial representation of the model should be adopted when initially explaining homeostasis, and it should be used to frame the discussion of the specific system being considered. Figure 1 shows such a diagram.

The argument could be made that this diagram may be difficult for undergraduate students to understand. This may be the rationale for presenting the much-simplified diagrams found in most undergraduate texts (17). However, because these simple diagrams do not explicitly include all components of a homeostatic regulatory system (e.g., a set point), they may be a source of the misconceptions discussed as sticky points. As a result, students may not recognize that an essential feature of homeostatic regulatory systems is minimizing an error signal. A simplified representation of the model that includes the critical components of the regulatory system is shown in Fig. 2 . Depending on the course content and level of the student, this model can be expanded to add more levels of complexity as are required.

Simplified representation of a homeostatic regulatory system. Several components shown in Fig. 1 are combined in this representation. The reader should refer to Table 1 to find correspondence between components of physiologically significant homeostatic regulatory systems and this simplified representation. For example, chemosensors in the carotid bodies and aortic body are “sensors,” the brain stem is the 𠇌ontrol center,” and the diaphragm and other respiratory muscles are �tors” in the homeostatic regulatory system for arterial P o 2.

3. Faculty members should introduce the concept of homeostatic regulation early in the course and continue to apply and hence reinforce the model as each new homeostatic system is encountered. It is important to continue to use the standard terminology and visual representation as recommended in the first and second points above. Students tend to neither spontaneously or readily generalize their use of core concepts. It is therefore incumbent on the instructor to create a learning environment where this kind of transfer behavior is promoted. Faculty members can facilitate this by providing multiple opportunities for students to test and refine their understanding of the core concept of homeostatic regulation.

One way to reinforce the broad application of the model of homeostasis and help students demonstrate that they understand any particular homeostatic mechanism is to have them ask (and answer) a series of questions about each of homeostatically regulated systems they encounter (see Table 3 ). In doing so, they demonstrate that they can determine the essential components of the mental model needed to define the homeostatic system. The effort to thoroughly and accurately answer these questions will help students uncover gaps in their understanding and will reveal uncertainties in the resource information that they are using.

Table 3.

Questions students should ask about any homeostatically regulated system

What is the homeostatically regulated variable? Is it a property or condition of the extracellular fluid?
What and where is the sensor?
What and where is the control center?
What and where is the effector(s)? How do they alter their activities so as to produce a response?
Does the response lead to a change in the regulated variable/stimulus consistent with error signal reduction (negative feedback)?

4. Faculty members should use care when they select and explain the physiological examples or analogical models they chose to introduce and illustrate homeostasis in the classroom. In particular, instructors should ensure that the representative examples they use do not introduce additional misconceptions into student thinking. This is especially so when thermoregulation may be considered as an example of homeostatic regulation.

An informal survey of physiology textbooks indicated that thermoregulation is almost universally used as an example of a homeostatic mechanism. The most likely reasons for this selection are that 1) there is an everyday, seemingly easy to understand process involving the regulation of air temperature in room or building (i.e., the operation of a furnace and an air conditioner) and 2) the body's physiological responses are commonly and obviously observable and/or experienced by the learner (sweating, shivering, and changes in skin coloration). However, based on our description of the typical homeostatic regulatory system, there are compelling reasons to recommend that caution be taken if thermoregulation is used as the initial and representative example of homeostasis.

Most concerning, the typical home heating and cooling system operates in a manner that is distinctly different from mechanisms of human thermoregulation. The effectors in most houses, the furnace and air conditioner, operate in a full-on/full-off manner. For example, when the temperature at the thermostat falls below the value that has been dialed in (the set point temperature), the furnace turns on and stays on at maximum output until the temperature returns to the set point value. However, this is not how the human thermoregulatory system functions or how other homeostatic mechanisms operate. One potential consequence of using this model system to illustrate a homeostatic system is the creation of a common student misconception that homeostatic mechanisms operate in an on/off manner (12, 24), a sticky point we have addressed above. Faculty members need to help students overcome this problem area if they chose to use thermoregulation as a representative example of homeostasis.

What alternatives might be recommended? We suggest the automobile cruise control as a helpful nonbiological analog for homeostasis. The use of cruise control is not an uncommon activity for students, and, as we have described previously, the operation of a cruise control is theoretically easy to understand. What about a physiological example to represent homeostasis? A review of Table 1 would suggest the insulin-mediated system for blood glucose regulation during the fed state has much to recommend it. Students are generally familiar with the particulars of the system from either previous coursework or from personal experience. Other systems are likely to be less accessible to the beginning student of physiology.

However, faculty members should be aware that blood glucose regulation is not without its downsides as a representative example of homeostatic regulation. It is not easy to identify or explain the operation of the glucose sensor, the set point, and the controller involved in glucose homeostasis. Furthermore, there is probably no widely understood analog to glucose regulation that can be easily drawn from everyday life. Neither cruise controls, navigation systems on airplanes, autofocuses on cameras or other common, nor everyday examples of servomechanisms fully correspond to the operation of the feedback system involved in regulating blood glucose during the fed state. This points out the tradeoffs that must be made when any particular example or model is adopted to represent homeostatic regulation. Recognizing this, the use of a physiological control system such as glucose regulation during the fed state, where the effectors operate continuously, seems preferable to thermoregulation as a representative example for teaching the concept of homeostatic regulation.

5. When discussing discussing organismal physiology, restrict the use of the term “homeostatic regulation” to mechanisms related to maintaining consistency of the internal environment (i.e., the ECF).

Adopting these five strategies will provide students with a consistent framework for building their own mental models of specific homeostatic mechanisms and will help them recognize the functional similarities among different homeostatic regulatory systems at the organismal level. Because of its widespread application to different systems in organismal biology, homeostasis is one of the most important unifying ideas in physiology (15, 16). To construct a robust and enduring understanding of this concept, students need the proper tools. By giving them a precise and consistent terminology and encouraging them to use a standardized pictorial representation of the homeostatic model, we enable them to build a proper foundation for comprehending homeostatic systems. By making students aware of the potential sources of confusion surrounding the concept of homeostasis, i.e., the sticky points, we help prevent their thinking from becoming misguided or out of square. By doing so, we set the stage for our students to develop an accurate understanding of a wide range of physiological phenomena and to arrive at an integrated sense of the “wisdom of the body.”


Material and Methods

Network Structure and Training

Networks had a 20 (input layer/sensory surface)–10 (hidden layer/interneuron)–20 (output layer/sensory map) structure with fully connected layers and trainable bias in the hidden and output layers. Each network was trained with an array of 4,000 input vectors (prey groups), with number of objects per vector following a normal random ( $mathrm,=10$ , $mathrm,=2$ ) or a uniform random distribution, sampled between 1 and 20, and position of objects within each vector always following a uniform random distribution. Objects in a vector were represented by 1's and the remaining empty space by 0's. Networks were trained for 1,000 epochs using sequential weight updating, and static weight arrays were chosen according to an early‐stopping procedure (Hecht‐Nielsen 1990). Within this procedure, test arrays were the same size as training arrays and employed the same sampling distribution, and static weight arrays were chosen at minimum test error in the training period. The task of networks during training was to reproduce each input vector in the output layer. To incorporate replication of networks into analysis, 52 networks were trained for each combination of training algorithm and input vector distribution. The same starting weight matrices (uniform random numbers between −1 and 1) and training input data were used to train networks using the different training algorithms.

The backpropagation procedure (Ackley et al. 1985) was run with a learning rate of 0.2 (optimized in pilot studies to give rapid and reliable convergence in 1,000 epochs) and binary sigmoid activation functions (defined below). The associative reward‐penalty learning rule (Mazzoni et al. 1991 Barto 1995) is one of a class of network‐training methods that contain procedures analogous to the reinforcement phenomenon in psychology (Pennartz 1997) and, unlike backpropagation, generally include features consistent with known phenomena in neurobiology. Biological features present in associative reward‐penalty and absent in backpropagation include a single feedback reinforcement signal to all connections in addition to the basic network architecture described above, Hebb‐like synapses, and probabilistic firing of neurons. Within associative reward‐penalty networks, inputs may be continuous, but hidden and output units are binary stochastic elements with pi, the probability of firing of the ith unit, defined by where g(x) is the binary sigmoid function $g( x) =1/ ( 1+mathrm,[ -x] ) $ , the jth unit provides input xj to the ith unit via the connection wij, and M is the number of inputs to the unit. During weight updating, the reinforcement signal is calculated from error between actual and desired output as $r=1-varepsilon $ with where k indexes the K output units in the network, $x^<*>_$ is the desired output of the kth unit in the output layer, $x_$ is its actual output, and n is a constant. Weights are then updated according to where xi is the output of the ith unit of the network, and ρ and λ are constants. Optimized values of $ ho =0.125$ , $lambda =0.0025$ , and $n=1.5$ were used on the basis of multiple estimates of error reduction over 100 epochs for combinations around the values of Mazzoni et al. (1991).

Using Static Networks to Generate Predictions: Prey‐Object Targeting

Targeting of a prey item within a group by static networks was simulated by projecting the target prey object onto a central position (position 10) of the input layer and determining the number of occasions (over 50 replicates for each treatment defined below, with positionally random nontarget prey) in which an object was registered as “present” at the same position of the sensory map. This was repeated for all trained networks. The choice of input position for the target is analogous to the tendency of many animals to focus objects of interest onto a central portion of the retina. For the binary associative reward‐penalty networks, a value of 1 at position 10 of the output layer indicated “object present,” and for the backpropagation networks (potentially continuous output), a value >0.8 was chosen because it gave analogous targeting‐accuracy versus group‐size relationships in networks trained with different algorithms (the remainder of parameter space produced patterns less consistent with the confusion effect). Network output data were predominantly nonnormal, and the median value ( $n=52$ ) of proportional target identification success ( $n=50$ ) was presented with 95% confidence intervals for the median (Zar 1999). The Kruskal‐Wallis test (Zar 1999) was used to test whether median artificial neural network targeting accuracy differed with respect to group size (the confusion effect), and the two‐way Scheirer‐Ray‐Hare extension of this test (Sokal and Rohlf 1995) was used to analyze treatment effects with respect to the confusion effect. The basic form of the confusion effect and factors that are known or suspected to alleviate it were investigated as follows.

The basic confusion effect. Fish, primates, birds, squid, and cuttlefish find it more difficult to capture individual prey as the number of prey items in the preyed on group increases (Gillett et al. 1974 Neill and Cullen 1974 Treherne and Foster 1982 Landeau and Terborgh 1986 Schradin 2000). To test for the confusion effect using our model, a target prey object with $mathrm,=1$ was projected onto position 10 of the trained network, and 1–19 objects with $mathrm,=1$ were placed at random positions around this target (replications as described above apply).

Alleviation of the confusion effect if the target is more visually intense than other group members. The “oddity effect” is considered a general phenomenon (Dukas 2002 Krause and Ruxton 2002) and has been experimentally demonstrated in bass and sticklebacks preying on minnows and water fleas (respectively), even when the relative conspicuousness of target and nontarget prey versus background is controlled for (Ohguchi 1978 Landeau and Terborgh 1986). It was investigated here by maintaining the target prey object at $mathrm,=1$ and giving all surrounding objects intensity $mathrm,=1$ , 0.75, 0.5, or 0.25. Each combination was repeated for the full range (1–20) of prey‐group sizes. To control for target/nontarget conspicuousness, procedures were repeated with nontargets of $mathrm,=1$ and 0.1 and background (previously called empty space) set to 0.55.

Targets are more vulnerable in heterogeneous‐looking than homogeneous‐looking groups. This is considered to be a general effect (Krause and Ruxton 2002) and has been experimentally demonstrated in bass preying on minnows (Landeau and Terborgh 1986). In this study, targets were maintained at $mathrm,=1$ and surrounding objects varied at random from $mathrm,=0.1$ to 1 at increments of 0.1. Again, this was repeated for the full range of group sizes.

A target isolated from the group is easier to capture than one in the center. Predators commonly try to isolate individuals from prey groups (Schaller 1972 Major 1978 Schmitt and Strand 1982), but the value of this behavior in alleviating the confusion effect has not been established (Krause and Ruxton 2002). To investigate this effect, the final seven positions of vectors created as in the basic confusion effect described above were sampled, two positions were left empty, and the target was projected onto position 10 as usual. This gave vectors representing a view of the end of a prey group with one isolated individual.

Compaction and the confusion effect. Some species of shoaling fish show compaction when at risk from predation (Seghers 1974 Magurran and Pitcher 1987), but it is not known whether this behavior worsens the confusion effect for predators (Krause and Ruxton 2002). The effect was investigated by creating vectors as described in the basic confusion effect above and comparing these to vectors in which the equivalent number of surrounding objects are completely compacted around the target, with no empty spaces between “nontarget prey.”

Model Validation with Experiments on Human Targeting

The model of the confusion effect was validated using “human predators” by constructing a computer interactive program that simulates a shoal or group of organisms “bursting” outward from a central point (similar to the flash‐expansion predator‐avoidance mechanism in fish Parrish et al. 2002) in which the task of users was to click with the mouse cursor an initially highlighted individual (fig. 1). Figure 1:

A computer interactive to quantify the confusion effect in humans, in four parts. During part 1, the mouse cursor is frozen in the middle of the computer screen while a countdown is shown. Part 2 shows the first frame of the interactive part of the simulation, in which the user begins his or her attempt to click the object indicated with an arrow. Between parts 2 and 3 are six frames in which the target object continues to be highlighted by a small arrow. During part 4, the arrow is removed, and the user must continue to attempt to strike the previously targeted object. The simulation is repeated with different numbers of objects between 1 and 100. Additional procedures are described in the text, and video footage (video 1) of the simulation in use, as well as Matlab code for the interactive, is available.

The simulation was run on a notebook computer with a 15‐inch LCD color monitor (60‐Hz refresh rate) and user‐defined viewing distance. Each simulation run was initiated by a visual countdown of 3 s and was confined to a $16 imes 16$ ‐cm square in the center of the screen, underneath which the mouse cursor was frozen in order to avoid prepositioning. A group of tadpole‐like prey items then appeared in a ring around the cursor (so that the user had to pursue a prey item), and the prey items moved outward for 0.24 s, with the prey item to be pursued highlighted by a small arrow. In the final and longest phase, the prey items continued to move outward, but the individual to be pursued was no longer highlighted. Unpredictability was added to the outward direction of prey movement by adding a random angular deviation from the previous direction, sampled from a normal random distribution with $mathrm,=0^$ and $mathrm,=5.7^$ . Frames were updated every 40 ms, and prey items moved at a speed of 2 cm/s. For color and dimensional details, see figure 1, video 1, and video footage and Matlab code for the interactive program. Video 1:

Computer interactive as controlled by a human user. The user, controlling the circular mouse cursor, attempts to capture on a computer screen an object initially highlighted with a red arrow.
Download video: video1.mpg (2.4 MB)

The task of the user was to click once on the “body” part of the initially highlighted prey item while the mouse cursor (over which the user had control) overlapped it and before all objects had left the screen. Users were allowed multiple clicks in their pursuit of the prey, and 1, 5, 10, 15, 20, 25, 30, 35, 40, 50, 60, 70, 80, 90, and 100 prey per group were run in a random presentation, with this procedure repeated four times per user. The 47 users were university staff members and students of both sexes between the ages of 19 and 54. They were unaware of the phenomenon under investigation until after they had participated. The confusion effect was quantified as the percentage of hits of the target prey at each group size ( $n=47$ ), and the median percentage ( $n=4$ ) was plotted against model output after normalization of user data to allow meaningful comparison with model output.

All procedures described in the methods section were coded and executed in the Matlab computer package (ver. 6.5, release 13), with the exception of Kruskal‐Wallis and Scheirer‐Ray‐Hare tests, which were run in SPSS (ver. 12.0.01). In addition to video footage (video 1) and Matlab code of the experimental computer interactive described above, code for network training and testing procedures is also available as supplementary information.


OBJECTIVES OF NERVOUS AND SENSORY SYSTEMS

1- Which of the following are the integrative systems in our body?

2. Nervous system in organisms, in general serve to

(a) regulate and control the activities of different organs in the body.

(b) link and coordinate the activities of various organs to ensure the intigrity of the animal.

(c) help the organs to maintain unity with the environment.

(a) afferent that carry impulses from periphery of the body to CNS.

(b) efferent that carry impulses from
CNS to the efferent organs.

5. The elements of nervous system which help in co-ordination are: •

(a) Diffused and ganglionic nervous system.

(b) Diffused and centralized nervous system.

7. Routing of signals to one of several alternative circuits, amplification of certain signals while reduction of others, integration of signals from diffuse sources, learning etc, are performed by?

(c) neuromuscular junctions

of one neuron or nerve axon ending of other

10. The electrical potential that cell membrane is exists across a

(a) resting membrane potential

(b) active membrane potential

(b) concentraction of dendrites and axons

(c) bundles of axons or dendrites of neurons.

(d) bundle of axons or dendrites bounded by connective tissue.

12. Which of these have excitability

.13-Which of these is a correct statement

(a) all of the neurons are excitable.

(b) all of the neurons can transmit impulses across their membrane.

(c) transmission of nerve impulses is always unidirectional.

(d) all of these statements

14. The impulses from sense organs are always carried from sense organs to CNS by means of

15. Impulses from CNS to effectors are always carried by

16. Dendrites of which type of neuron conduct impulses towards cellbody?

17. Conduction of nerve impulse through a nerve fibre is purely

(c) an electrochemical phenomenon

18. An impulse travels along the nerve fibre as a

(a) self propagative wave of some electrochemical changes.

(b) self propagative wave of mechanical changes.

(c) self propagative wave of thermal changes.

(d) self propagative wave of none of these changes.

19. Conduction of nerve impulse depends upon

(a) Permeability of surface membrane of axon

(c) electric equivalence between axoplasm and extra cellular fluid.

20. Under the condition of disturbed permeability of surface membrane of axon the nerve impulse will

(d) conduct first slowly then fastly.

21. How can we disturb the conduction of impulse through a nerve fibre?

(a) by disturbing the permeability of surface membrane of axon

(b) by altering the oxmotic equilibrium.

(c) by disturbing the electrical equivalence

(d) by all of these processes.

22. Synapse is a gap between adjacent

(d) nerve cell and other cell.

23. An impulse will travel through a nerve fibre only if the membrane becomes more permeable to ions of

24. Nerve impulse is, infact, a process which is associated with which of these phenomenon.

25. A nerve which conducts impulses from a tissue to nerve is called

26. A synpase at which local currents resulting from electrical activity flow between two neurons through gap junctions joining them is called

27. Afferent nerve fibres conduct impulses from

28. During conduction of an impulse, electric potential on inside of axolemma (plasma membrane of axon) changes from.

(a) negative to positive and remain • positive.

(b) negative to positive and remain negative.

(c) positive to negative and remain positive.

(d) positive to positive and remain negative.

29. In the resting stage the axolemma is

(a) poorly permeable to Na+ ions

(b) quite permeable to K ± and Cl – ions

(c) impermeable to all these ions

30. In resting stage the axolemma is poorly premeable to Na + ions but quite

permeable to e and CI ions by

31. Sodium – potassium pump means

(a) Expelling of Na + into extracellular

fluid and intake of e from cytoplasm against concentration gradient.

(b) Expelling of le into extracellular

fluid and intake of Na + from cytoplasm

(c) Only expelling of Na + into extracellular fluid

(d) Only intake of ic f into cytoplasm.

32. Sodium – potassium – pump operates with the help of which of these enzymes.

33. The negative charges over complex organic molecules are neutralized by

34. Sodium-potassium-pump functions mainly to

(a) maintain osmotic equilibrium between
extracellular fluid and cytoplasm.

(b) reduce the charges over surface membrane.

(c) to speed up the propagation of nerve impulse.

35. Each cell in resting stage is in polarized state with a membrane potential of

36. The electric potential across membrane of each resting cell is

(c) resting membrane potential

37. Saltatory transmission of nerve impulse occurs in the

38. Synapses between motor fibers and end plates are called.

(c) neurosecretory synapses.

39. Cholinergic fibers are those which liberate at their free ends.

40. Which of these is not a neurohormone.

41. Neurohormones inhibiting post-synaptic transmission are

42. Acetylcholine is responsible for transmission of nerve impulses through

43. Destruction of acetylcholine by acetylcholinesterase is required
because of

(a) the pesence of acetylcholine on dendrites which will continue to transmit the same impulse.

(b) it will make farther transmission impossible. (c) both of a and b

(a) neuro transmittor across synapses.

45. The synapse between two neurons may be

46. Most primitive nervous system is found in

47. Which of these has a nervous system but no brain

48. The neuron net of Hydra lacks

(d) direction of impulse flow

(a) sensory cells but no nerve cells.

(b) both sensory and nerve cells.

(c) neither sensory nor nerve cells.

(d) nerve cells but no sensory cells.

50. Nervous system of Hydra is made up of

(c) ganglionated nerve cords.

51. Nervous system in Hydra is formed by.

52-Number of subpharyngeal ganglia in earthworm is

(c) two pairs (d) three pairs

53-Subphatyngeal ganglia in earth worm supply nerves to

(b) anterior three segments

54-In earthworms ventral nerve cord has symmetrical ganglia

(a) in all segments of body

(b) in all segments behind 4 th segment

(d) all segments behind clitellum.

55. One segmental ganglia gives out

56-Nerve cord of cockroach consists of which of these numbers of ganglia

57. Nerves to mandibles in cockroach are given by

(b) circumoesophageal connective.

(c) suboespophageal ganglia k frontal ganglia

58-First thoracic ganglia in cockroach gives which number of the nerves

(a) two pairs (b) three pairs

59. Last abdominal ganglia in cockroach gives out which of these number of nerves

60. Nervous system in vertebrates consists of

(b) autonomic nervous system

(c) peripheral nervous system

61. Which one of the following is supreme controller of total body responses.

(a) autonomic nervous system

(c) peripheral nervous system

62. The alkaline and lymph-like serous fluid present inside the cavity of brain and spinal cord is called.

63. Extending from the spinal cord in frog are

(d) dorsal and ventral nerve roots

64. Brain and spinal cord in frog are covered with which of the following meniges.

(c) both of these (d) none of
these

65. Arachnoid is present between.

(b) dura mater and the sheath of overlying bone.

66. Ventricles present in cerebral hemispheres are called.

(c) both of these (d) none of
these

67. Space inside the olfactory lobes is called

68. Communication between two paracoels is called

69. Cavity within the spinal cord is called

(c) enterocoel (d) schizocoel.

70. The active ingredient in most flea sprays and powders is parathion which prevents breakdown of

71. Outermost covering meninx of brain is.

(c) duramater (d) all of these

72. Cerebral hemispheres are centres of

73. HypothalamuS is formed by

(a) ventral wall of diencephalon

(a) fore brain with mid brain

(b) mid brain with hind brain.

(c) fore brain with hind brain

(d) hind brain with spinal cord.

75. Which groups have cerebellum larger than other groups.

76. Which animal’ group has usually a rudimentary crebellum reflecting their simple locomotory pattern.

77. Seat of highest mental faculties like nature are consciousness, intelligence and articulate speech in the brain is


Reflex Arcs

Reflex arcs are an interesting phenomenon for considering how the PNS and CNS work together. Reflexes are quick, unconscious movements, like automatically removing a hand from a hot object. Reflexes are so fast because they involve local synaptic connections in the spinal cord, rather than relay of information to the brain. For example, the knee reflex that a doctor tests during a routine physical is controlled by a single synapse between a sensory neuron and a motor neuron. While a reflex may only require the involvement of one or two synapses, synapses with interneurons in the spinal column transmit information to the brain to convey what happened after the event is already over (the knee jerked, or the hand was hot). So this means that the brain is not involved at all in the movement associated with the reflex, but it is certainly involved in learning from the experience – most people only have to touch a hot stove once to learn that they should never do it again!

The simplest neuronal circuits are those that underlie muscle stretch responses, such as the knee-jerk reflex that occurs when someone hits the tendon below your knee (the patellar tendon) with a hammer. Tapping on that tendon stretches the quadriceps muscle of the thigh, stimulating the sensory neurons that innervate it to fire. Axons from these sensory neurons extend to the spinal cord, where they connect to the motor neurons that establish connections with (innervate) the quadriceps. The sensory neurons send an excitatory signal to the motor neurons, causing them to fire too. The motor neurons, in turn, stimulate the quadriceps to contract, straightening the knee. In the knee-jerk reflex, the sensory neurons from a particular muscle connect directly to the motor neurons that innervate that same muscle, causing it to contract after it has been stretched. Image credit: https://www.khanacademy.org/science/biology/ap-biology/human-biology/neuron-nervous-system/a/overview-of-neuron-structure-and-function, modified from “Patellar tendon reflex arc,” by Amiya Sarkar (CC BY-SA 4.0). The modified image is licensed under a CC BY-SA 4.0 license.

This video provides an overview of how reflex arcs work: