Ganglia are collections, or small knots, of nerve cell bodies outside the CNS. The peripheral nervous system is further subdivided into an afferent sensory division and an efferent motor division.
The afferent or sensory division transmits impulses from peripheral organs to the CNS. The efferent or motor division transmits impulses from the CNS out to the peripheral organs to cause an effect or action. Finally, the efferent or motor division is again subdivided into the somatic nervous system and the autonomic nervous system.
The somatic nervous system, also called the somatomotor or somatic efferent nervous system, supplies motor impulses to the skeletal muscles. Because these nerves permit conscious control of the skeletal muscles, it is sometimes called the voluntary nervous system. If you swallow a large bolus of food, for instance, you will probably feel the lump of that food as it pushes through your esophagus, or even if your stomach is distended after a large meal.
If you inhale especially cold air, you can feel it as it enters your larynx and trachea. These sensations are not the same as feeling high blood pressure or blood sugar levels. When particularly strong visceral sensations rise to the level of conscious perception, the sensations are often felt in unexpected places.
For example, strong visceral sensations of the heart will be felt as pain in the left shoulder and left arm. This irregular pattern of projection of conscious perception of visceral sensations is called referred pain. Depending on the organ system affected, the referred pain will project to different areas of the body Figure 2.
Referred Pain Chart. The location of referred pain is not random, but a definitive explanation of the mechanism has not been established.
The most broadly accepted theory for this phenomenon is that the visceral sensory fibers enter into the same level of the spinal cord as the somatosensory fibers of the referred pain location.
By this explanation, the visceral sensory fibers from the mediastinal region, where the heart is located, would enter the spinal cord at the same level as the spinal nerves from the shoulder and arm, so the brain misinterprets the sensations from the mediastinal region as being from the axillary and brachial regions. Projections from the medial and inferior divisions of the cervical ganglia do enter the spinal cord at the middle to lower cervical levels, which is where the somatosensory fibers enter.
The spleen is in the upper-left abdominopelvic quadrant, but the pain is more in the shoulder and neck. How can this be? The sympathetic fibers connected to the spleen are from the celiac ganglion, which would be from the mid-thoracic to lower thoracic region whereas parasympathetic fibers are found in the vagus nerve, which connects in the medulla of the brain stem. However, the neck and shoulder would connect to the spinal cord at the mid-cervical level of the spinal cord.
These connections do not fit with the expected correspondence of visceral and somatosensory fibers entering at the same level of the spinal cord. The incorrect assumption would be that the visceral sensations are coming from the spleen directly. In fact, the visceral fibers are coming from the diaphragm. The nerve connecting to the diaphragm takes a special route. The phrenic nerve is connected to the spinal cord at cervical levels 3 to 5.
The motor fibers that make up this nerve are responsible for the muscle contractions that drive ventilation.
These fibers have left the spinal cord to enter the phrenic nerve, meaning that spinal cord damage below the mid-cervical level is not fatal by making ventilation impossible.
Therefore, the visceral fibers from the diaphragm enter the spinal cord at the same level as the somatosensory fibers from the neck and shoulder. When the spleen ruptures, blood spills into this region. The accumulating hemorrhage then puts pressure on the diaphragm. The visceral sensation is actually in the diaphragm, so the referred pain is in a region of the body that corresponds to the diaphragm, not the spleen.
The efferent branch of the visceral reflex arc begins with the projection from the central neuron along the preganglionic fiber. This fiber then makes a synapse on the ganglionic neuron that projects to the target effector.
The effector organs that are the targets of the autonomic system range from the iris and ciliary body of the eye to the urinary bladder and reproductive organs. The thoracolumbar output, through the various sympathetic ganglia, reaches all of these organs.
The cranial component of the parasympathetic system projects from the eye to part of the intestines. The sacral component picks up with the majority of the large intestine and the pelvic organs of the urinary and reproductive systems. Somatic reflexes involve sensory neurons that connect sensory receptors to the CNS and motor neurons that project back out to the skeletal muscles.
Visceral reflexes that involve the thoracolumbar or craniosacral systems share similar connections. However, there are reflexes that do not need to involve any CNS components. A long reflex has afferent branches that enter the spinal cord or brain and involve the efferent branches, as previously explained. A short reflex is completely peripheral and only involves the local integration of sensory input with motor output Figure 3.
Short and Long Reflexes. The difference between short and long reflexes is in the involvement of the CNS. Somatic reflexes always involve the CNS, even in a monosynaptic reflex in which the sensory neuron directly activates the motor neuron.
That synapse is in the spinal cord or brain stem, so it has to involve the CNS. However, in the autonomic system there is the possibility that the CNS is not involved. If a sensory neuron projects directly to the ganglionic neuron and causes it to activate the effector target, then the CNS is not involved. A division of the nervous system that is related to the autonomic nervous system is the enteric nervous system.
The word enteric refers to the digestive organs, so this represents the nervous tissue that is part of the digestive system. There are a few myenteric plexuses in which the nervous tissue in the wall of the digestive tract organs can directly influence digestive function.
If stretch receptors in the stomach are activated by the filling and distension of the stomach, a short reflex will directly activate the smooth muscle fibers of the stomach wall to increase motility to digest the excessive food in the stomach.
No CNS involvement is needed because the stretch receptor is directly activating a neuron in the wall of the stomach that causes the smooth muscle to contract. That neuron, connected to the smooth muscle, is a postganglionic parasympathetic neuron that can be controlled by a fiber found in the vagus nerve. The autonomic nervous system is important for homeostasis because its two divisions compete at the target effector.
The balance of homeostasis is attributable to the competing inputs from the sympathetic and parasympathetic divisions dual innervation. At the level of the target effector, the signal of which system is sending the message is strictly chemical. A signaling molecule binds to a receptor that causes changes in the target cell, which in turn causes the tissue or organ to respond to the changing conditions of the body.
The postganglionic fibers of the sympathetic and parasympathetic divisions both release neurotransmitters that bind to receptors on their targets. Postganglionic sympathetic fibers release norepinephrine, with a minor exception, whereas postganglionic parasympathetic fibers release ACh. For any given target, the difference in which division of the autonomic nervous system is exerting control is just in what chemical binds to its receptors.
The target cells will have adrenergic and muscarinic receptors. If norepinephrine is released, it will bind to the adrenergic receptors present on the target cell, and if ACh is released, it will bind to the muscarinic receptors on the target cell.
In the sympathetic system, there are exceptions to this pattern of dual innervation. The postganglionic sympathetic fibers that contact the blood vessels within skeletal muscle and that contact sweat glands do not release norepinephrine, they release ACh.
This does not create any problem because there is no parasympathetic input to the sweat glands. Sweat glands have muscarinic receptors and produce and secrete sweat in response to the presence of ACh.
At most of the other targets of the autonomic system, the effector response is based on which neurotransmitter is released and what receptor is present. For example, regions of the heart that establish heart rate are contacted by postganglionic fibers from both systems. If norepinephrine is released onto those cells, it binds to an adrenergic receptor that causes the cells to depolarize faster, and the heart rate increases.
If ACh is released onto those cells, it binds to a muscarinic receptor that causes the cells to hyperpolarize so that they cannot reach threshold as easily, and the heart rate slows. Without this parasympathetic input, the heart would work at a rate of approximately beats per minute bpm. The sympathetic system speeds that up, as it would during exercise, to — bpm, for example. The parasympathetic system slows it down to the resting heart rate of 60—80 bpm.
Another example is in the control of pupillary size Figure 4. Autonomic Control of Pupillary Size. The afferent branch responds to light hitting the retina. Photoreceptors are activated, and the signal is transferred to the retinal ganglion cells that send an action potential along the optic nerve into the diencephalon.
If light levels are low, the sympathetic system sends a signal out through the upper thoracic spinal cord to the superior cervical ganglion of the sympathetic chain.
The postganglionic fiber then projects to the iris, where it releases norepinephrine onto the radial fibers of the iris a smooth muscle. When those fibers contract, the pupil dilates—increasing the amount of light hitting the retina. If light levels are too high, the parasympathetic system sends a signal out from the Eddinger—Westphal nucleus through the oculomotor nerve. This fiber synapses in the ciliary ganglion in the posterior orbit. The postganglionic fiber then projects to the iris, where it releases ACh onto the circular fibers of the iris—another smooth muscle.
When those fibers contract, the pupil constricts to limit the amount of light hitting the retina. In this example, the autonomic system is controlling how much light hits the retina.
It is a homeostatic reflex mechanism that keeps the activation of photoreceptors within certain limits. In the context of avoiding a threat like the lioness on the savannah, the sympathetic response for fight or flight will increase pupillary diameter so that more light hits the retina and more visual information is available for running away. Likewise, the parasympathetic response of rest reduces the amount of light reaching the retina, allowing the photoreceptors to cycle through bleaching and be regenerated for further visual perception; this is what the homeostatic process is attempting to maintain.
Organ systems are balanced between the input from the sympathetic and parasympathetic divisions. When something upsets that balance, the homeostatic mechanisms strive to return it to its regular state.
For each organ system, there may be more of a sympathetic or parasympathetic tendency to the resting state, which is known as the autonomic tone of the system. For example, the heart rate was described above. Because the resting heart rate is the result of the parasympathetic system slowing the heart down from its intrinsic rate of bpm, the heart can be said to be in parasympathetic tone. In a similar fashion, another aspect of the cardiovascular system is primarily under sympathetic control.
Blood pressure is partially determined by the contraction of smooth muscle in the walls of blood vessels. These tissues have adrenergic receptors that respond to the release of norepinephrine from postganglionic sympathetic fibers by constricting and increasing blood pressure.
The hormones released from the adrenal medulla—epinephrine and norepinephrine—will also bind to these receptors. Those hormones travel through the bloodstream where they can easily interact with the receptors in the vessel walls.
The parasympathetic system has no significant input to the systemic blood vessels, so the sympathetic system determines their tone. There are a limited number of blood vessels that respond to sympathetic input in a different fashion. Blood vessels in skeletal muscle, particularly those in the lower limbs, are more likely to dilate.
It does not have an overall effect on blood pressure to alter the tone of the vessels, but rather allows for blood flow to increase for those skeletal muscles that will be active in the fight-or-flight response. The blood vessels that have a parasympathetic projection are limited to those in the erectile tissue of the reproductive organs.
Acetylcholine released by these postganglionic parasympathetic fibers cause the vessels to dilate, leading to the engorgement of the erectile tissue. Have you ever stood up quickly and felt dizzy for a moment?
This is because, for one reason or another, blood is not getting to your brain so it is briefly deprived of oxygen. When you change position from sitting or lying down to standing, your cardiovascular system has to adjust for a new challenge, keeping blood pumping up into the head while gravity is pulling more and more blood down into the legs.
The reason for this is a sympathetic reflex that maintains the output of the heart in response to postural change. When a person stands up, proprioceptors indicate that the body is changing position.
A signal goes to the CNS, which then sends a signal to the upper thoracic spinal cord neurons of the sympathetic division. The sympathetic system then causes the heart to beat faster and the blood vessels to constrict. Both changes will make it possible for the cardiovascular system to maintain the rate of blood delivery to the brain. Blood is being pumped superiorly through the internal branch of the carotid arteries into the brain, against the force of gravity.
Gravity is not increasing while standing, but blood is more likely to flow down into the legs as they are extended for standing. This sympathetic reflex keeps the brain well oxygenated so that cognitive and other neural processes are not interrupted.
Sometimes this does not work properly. If the sympathetic system cannot increase cardiac output, then blood pressure into the brain will decrease, and a brief neurological loss can be felt. The name for this is orthostatic hypotension, which means that blood pressure goes below the homeostatic set point when standing. There are two basic reasons that orthostatic hypotension can occur. First, blood volume is too low and the sympathetic reflex is not effective.
This hypovolemia may be the result of dehydration or medications that affect fluid balance, such as diuretics or vasodilators. Both of these medications are meant to lower blood pressure, which may be necessary in the case of systemic hypertension, and regulation of the medications may alleviate the problem.
Sometimes increasing fluid intake or water retention through salt intake can improve the situation. The second underlying cause of orthostatic hypotension is autonomic failure. There are several disorders that result in compromised sympathetic functions. The disorders range from diabetes to multiple system atrophy a loss of control over many systems in the body , and addressing the underlying condition can improve the hypotension.
For example, with diabetes, peripheral nerve damage can occur, which would affect the postganglionic sympathetic fibers. Getting blood glucose levels under control can improve neurological deficits associated with diabetes. Autonomic nervous system function is based on the visceral reflex. This reflex is similar to the somatic reflex, but the efferent branch is composed of two neurons. The central neuron projects from the spinal cord or brain stem to synapse on the ganglionic neuron that projects to the effector.
The afferent branch of the somatic and visceral reflexes is very similar, as many somatic and special senses activate autonomic responses.
However, there are visceral senses that do not form part of conscious perception. If a visceral sensation, such as cardiac pain, is strong enough, it will rise to the level of consciousness. However, the sensory homunculus does not provide a representation of the internal structures to the same degree as the surface of the body, so visceral sensations are often experienced as referred pain, such as feelings of pain in the left shoulder and arm in connection with a heart attack.
The role of visceral reflexes is to maintain a balance of function in the organ systems of the body. The two divisions of the autonomic system each play a role in effecting change, usually in competing directions.
The sympathetic system increases heart rate, whereas the parasympathetic system decreases heart rate. The sympathetic system dilates the pupil of the eye, whereas the parasympathetic system constricts the pupil. The competing inputs can contribute to the resting tone of the organ system.
Heart rate is normally under parasympathetic tone, whereas blood pressure is normally under sympathetic tone. The heart rate is slowed by the autonomic system at rest, whereas blood vessels retain a slight constriction at rest. In a few systems of the body, the competing input from the two divisions is not the norm. The sympathetic tone of blood vessels is caused by the lack of parasympathetic input to the systemic circulatory system.
Only certain regions receive parasympathetic input that relaxes the smooth muscle wall of the blood vessels. Sweat glands are another example, which only receive input from the sympathetic system. The pupillary light reflex Figure 1. Pupillary Reflex Pathways begins when light hits the retina and causes a signal to travel along the optic nerve.
This is visual sensation, because the afferent branch of this reflex is simply sharing the special sense pathway. Bright light hitting the retina leads to the parasympathetic response, through the oculomotor nerve, followed by the postganglionic fiber from the ciliary ganglion, which stimulates the circular fibers of the iris to contract and constrict the pupil.
When light hits the retina in one eye, both pupils contract. When that light is removed, both pupils dilate again back to the resting position. When the stimulus is unilateral presented to only one eye , the response is bilateral both eyes. The same is not true for somatic reflexes. If you touch a hot radiator, you only pull that arm back, not both. Central control of autonomic reflexes is different than for somatic reflexes.
The hypothalamus, along with other CNS locations, controls the autonomic system. Autonomic control is based on the visceral reflexes, composed of the afferent and efferent branches. These homeostatic mechanisms are based on the balance between the two divisions of the autonomic system, which results in tone for various organs that is based on the predominant input from the sympathetic or parasympathetic systems. Coordinating that balance requires integration that begins with forebrain structures like the hypothalamus and continues into the brain stem and spinal cord.
The hypothalamus is the control center for many homeostatic mechanisms. It regulates both autonomic function and endocrine function. The roles it plays in the pupillary reflexes demonstrates the importance of this control center.
The optic nerve projects primarily to the thalamus, which is the necessary relay to the occipital cortex for conscious visual perception. Another projection of the optic nerve, however, goes to the hypothalamus.
The hypothalamus then uses this visual system input to drive the pupillary reflexes. If the retina is activated by high levels of light, the hypothalamus stimulates the parasympathetic response. If the optic nerve message shows that low levels of light are falling on the retina, the hypothalamus activates the sympathetic response. Output from the hypothalamus follows two main tracts, the dorsal longitudinal fasciculus and the medial forebrain bundle Figure 2.
Fiber Tracts of the Central Autonomic System. Along these two tracts, the hypothalamus can influence the Eddinger—Westphal nucleus of the oculomotor complex or the lateral horns of the thoracic spinal cord. These two tracts connect the hypothalamus with the major parasympathetic nuclei in the brain stem and the preganglionic central neurons of the thoracolumbar spinal cord.
The hypothalamus also receives input from other areas of the forebrain through the medial forebrain bundle. The olfactory cortex, the septal nuclei of the basal forebrain, and the amygdala project into the hypothalamus through the medial forebrain bundle. These forebrain structures inform the hypothalamus about the state of the nervous system and can influence the regulatory processes of homeostasis. A good example of this is found in the amygdala, which is found beneath the cerebral cortex of the temporal lobe and plays a role in our ability to remember and feel emotions.
The amygdala is a group of nuclei in the medial region of the temporal lobe that is part of the limbic lobe Figure 3. The Limbic Lobe. The limbic lobe includes structures that are involved in emotional responses, as well as structures that contribute to memory function. The limbic lobe has strong connections with the hypothalamus and influences the state of its activity on the basis of emotional state.
For example, when you are anxious or scared, the amygdala will send signals to the hypothalamus along the medial forebrain bundle that will stimulate the sympathetic fight-or-flight response. The hypothalamus will also stimulate the release of stress hormones through its control of the endocrine system in response to amygdala input. The medulla contains nuclei referred to as the cardiovascular center , which controls the smooth and cardiac muscle of the cardiovascular system through autonomic connections.
When the homeostasis of the cardiovascular system shifts, such as when blood pressure changes, the coordination of the autonomic system can be accomplished within this region.
Furthermore, when descending inputs from the hypothalamus stimulate this area, the sympathetic system can increase activity in the cardiovascular system, such as in response to anxiety or stress. The preganglionic sympathetic fibers that are responsible for increasing heart rate are referred to as the cardiac accelerator nerves , whereas the preganglionic sympathetic fibers responsible for constricting blood vessels compose the vasomotor nerves. Several brain stem nuclei are important for the visceral control of major organ systems.
One brain stem nucleus involved in cardiovascular function is the solitary nucleus. It receives sensory input about blood pressure and cardiac function from the glossopharyngeal and vagus nerves, and its output will activate sympathetic stimulation of the heart or blood vessels through the upper thoracic lateral horn. The mammillotegmental tract is less prominent than either the DLF or MFB nevertheless, this pathway that originates in the mammillary nucleus sends projections into the mesencephalic and pontine reticular formations that in turn influence the activity of the brainstem autonomic nuclei listed above.
As noted above, the central autonomic network consists of three hierarchically ordered circuits or loops: the short-term brainstem-spinal loops, and the limbic brain-hypothalamic-brainstem-spinal cord loops mediating anticipatory and stress responses, and the intermediate length hypothalamic-brainstem-spinal cord loops mediating longer-term autonomic reflexes. Here we focus on this later loop in its role in thermoregulation. A later chapter will focus on this loop in the regulation of feeding.
Regulation of core temperature is essential because most of the metabolic processes necessary for life are strongly temperature-dependent. The normal body temperature set-point is primarily determined by the activity of neurons in the medial preoptic and anterior hypothalamic nuclei as well as by neurons in the adjoining medial septal nuclei.
Collectively this region is often termed the preoptic anterior hypothalamus POAH. The second region that also plays a critical, though subservient role to the POAH, in temperature regulation is the posterior hypothalamus.
It was previously mentioned that the hypothalamus is one of the few brain areas where CNS neurons reside that are themselves directly sensitive to physical or chemical variables such as temperature, plasma osmolality, plasma glucose, and various hormones. The POAH has three types of neurons involved in determining the temperature set-point, warm-sensitive neurons, cold-sensitive neurons, and temperature-insensitive neurons, that are defined by changes in discharge rate following local warming or cooling of the POAH.
These neurons have a firing rate versus temperature as shown in Figure 3. Change in temperature below 37 degrees has little effect on discharge rate. However, as temperature rises above 37 degrees the discharge rate of these neurons increases dramatically. Activation of warm-sensitive neurons results in an activation of neurons in the paraventricular nucleus PVN and lateral hypothalamus that result in heightened parasympathetic outflow to promote the dissipation of heat.
The cold-sensitive neurons show low rates of discharge at temperatures above 37 degrees, but increase firing rate steeply as temperature is lowered below 37 degrees. Increased discharges in cold-sensitive neurons results in activation of neurons in the PVN and the posterior hypothalamus that increase sympathetic outflow to promote the generation and conservation of heat.
The final group of neurons found in the POAH and posterior hypothalamus is the temperature-insensitive neurons. These are by-far the most numerous of the neurons in these nuclei, comprising greater than 60 percent of those in the POAH.
Click the octagon shapes. The master circuit in regulation of body temperature is heat dissipation. The warm-sensitive neurons of the POAH have intrinsic membrane receptors that are sensitive to changes in brain and blood temperature above 37 degrees. These are non-specific cation channels that very likely are related to the vanilloid capsaicin-sensitive family of thermoreceptors.
Warm-sensitive neurons also receive excitatory inputs from cutaneous and spinal thermoreceptors. As illustrated in Figure 3. Interestingly, though the firing rate of these cells continues to increase with increases in body temperature, the slope of this increase is reduced. Thus, the drive to dissipate heat is actively driven by inputs from thermal receptors.
It is not clear that such is the case for heat generation and conservation. Cool-sensitive neurons do not appear to have intrinsic temperature-sensitive receptors.
Rather, the increase in discharge observed in cool-sensitive cells with cooling results from the decreases in discharge of the warm-sensitive neurons and subsequent disinhibition so that the cool-sensitive neurons are now driven by tonic inputs from the thermal-insensitive neurons. Thus, the temperature set-point is principally a function of activity in warm-sensitive neurons of the POAH.
The short-term effects of output from both warm- and cool-sensitive neurons on body temperature occur as a result of changes in autonomic tone to cutaneous arterioles and so the amount of cutaneous blood flow. Changes in sympathetic outflow to sweat glands and adipose tissue provide additional targets used for heat dissipation and generation.
Longer-term effects of these groups of neurons in response to sustained changes in environmental temperature include the induction of behavioral and neuroendocrine responses to changes in environmental temperature. The statement above highlights well the fact that fever has been a scourge battled by physicians since antiquity. The sickness response includes behavioral, cognitive, metabolic, and neuroendocrine adaptations that are all geared to make the body less hospitable to pathogens and most primed for optimizing immunological defenses.
Thus, fever is initiated because most bacteria proliferate poorly at temperatures above 39 degrees, whereas the function of lymphoid cells is optimal at this temperature. Fever is initiated during infection following the activation of macrophages and the subsequent synthesis and release of endogenous pyrogenic substances including interleukin-1 IL-1 , tumor necrosis factor TNF , interleukin-6 IL-6 , and the interferons IFN.
The increased cAMP activates the protein kinase A system resulting in reduced excitability of the warm-sensitive neurons and lowering of their discharge rate. This allows the discharge rate of the cool-sensitive neurons to increase thus, establishing a new, higher temperature set-point. The use of antipyretics such as aspirin and indomethacin counteracts fever by interrupting the synthesis of PGE2 through antagonism of the cyclooxygenase enzyme system in the endothelium of the OVLT.
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