The Nervous System - Advanced Version / Functions of the Nervous System

submitted by Dr. Gary Farr Last Updated June, 24, 2002

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Cerebellum

Although a cycle of simple repetitive movements can be organized without sensory feedback, more sophisticated movements require feedback as well as what is called feed-forward control. This is provided by the cerebellum. Many parts of the brain have to be kept informed of movements being carried out in order to detect error and continually correct the movement. The cerebellum continuously receives inputs from the trunk, limbs, eyes, ears, and vestibular apparatus, maintaining in turn a continuous transfer of information to the motor parts of the thalamus and to the cerebral cortex.

As a movement is being prepared, a replica of the instructions is sent to the cerebellum; the cerebellum sends back its own information to the cortex. The cortex, meanwhile, sends information about the movement to various afferent neurons that are about to receive information from receptors in the body parts where the movement is about to begin. This comparison between instructions sent and movement performed is a fundamental requirement of all complicated movement. The discharge of impulses from motor to sensory regions is called the corollary discharge. The mechanisms involving the cerebellum do not come to consciousness. There are no sensory consequences of damage to the cerebellum, for the cerebellum is a motor structure.

As series of movements are learned and improved with practice, a replica of the movement is probably retained in the cerebral hemispheres. (The mechanisms of this postulated “replica” are as yet unknown.) Whenever the learned movements are repeated, they are formed and guided by the replica. This hypothesis of controlling movement by previously practiced patterns was developed by von Holst. He gave the name efference to the totality of motor impulses necessary for a movement, and he proposed that whenever the efference is produced it leaves an image of itself somewhere in the central nervous system. This image he called the efference copy. According to von Holst's theory, as the movement is repeated, afferent impulses return to the brain from receptors activated by muscular activity. These impulses are called the re-afference. There is then a comparison between the efference copy and the re-afference. When they are identical, the movement is “correct” in relation to its previous performance. When the re-afference differs from the efference copy, corrections have to be made so as to bring the present pattern of movement back to the original image left in the brain.

If the cerebellum is damaged or degenerates, any error between the movement being performed and the efference copy will no longer be corrected, and the postural adjustments sent from the cerebral hemispheres will no longer be implemented. The force and extent of movements also will be abnormal, the movement going too far or not far enough. The various muscles may not come into play at the right time, and there will be a disturbance in the relationship of antagonist muscles, so that the accurate arrival on target will be replaced by oscillation.

Basal ganglia

Most of what is known about the contribution of the basal ganglia has been obtained from studying abnormal conditions that occur when these nuclei are affected by disease. In Parkinson's disease there is a loss of the pigmented neurons of the substantia nigra, which release the neurotransmitter dopamine at synapses in the basal ganglia. Patients with this disease have a certain type of muscle stiffness called rigidity, a typical tremor, flexed posture, and difficulty in maintaining equilibrium. They have difficulty in starting movements, including walking, and they cannot put adequate force into fast movements. They have particular difficulty in changing from one movement to its opposite, in carrying out two movements simultaneously, and in stopping one movement while starting another.

The organization of posture, which is based on vestibular, proprioceptive, and visual input to the globus pallidus, is severely damaged when this region of the basal ganglia degenerates. As a changing posture of the various parts of the body is a prerequisite of every movement, this factor alone upsets all movement. Visual reflexes contributing to motion also act through the globus pallidus. When this structure is degenerate, what the patient sees may affect his ability to move. One patient may be unable to go forward if he has to pass through a narrow door, another may not be able to do so if he has to go into a wide expanse like a field.

The vestibular system

Animals have evolved sophisticated sensory receptors to detect features of the environment in which they live. In addition to the special senses such as hearing and sight, there are unobtrusive sensory systems such as the vestibular system, which is sensitive to acceleration.

Acceleration can be considered as occurring in two forms—linear and angular. One familiar type of linear acceleration is gravity. Because this environmental feature, unlike any other encountered by an organism, is always present, highly sophisticated systems have developed to detect gravity and enable an animal to maintain its position relative to the earth. A common form of angular acceleration is that induced by rotation, such as a turning of the head. Through the vestibular apparatus these forces are detected and appropriate motor activities are organized to counter the postural perturbations that they induce.

Receptors

The vestibular sensory organ is a paired structure located symmetrically on either side of the head within the inner ear. Inside each end organ are the hair cells, the detection units for both linear and angular acceleration. Extending from one surface of each hair cell are fine, hairlike cilia, displacement of which alters the electrical potential of the cell. Bending the cilia in one direction causes the cell membrane to depolarize while hyperpolarization is induced by movement in the opposite direction. Changes in membrane potential induce alteration in the firing of nerve impulses by the afferent neurons supplying each hair cell.

The two types of acceleration are detected by two types of vestibular end organ. Linear acceleration is sensed by a pair of organs—the saccule and utricle—while there are three receptor organs—called semicircular canals—in each vestibular apparatus for the detection of angular acceleration. For more information see the ear.

Saccule and utricle

Each saccule and utricle has a single cluster, or macula, of hair cells located in the vertical and horizontal planes, respectively. Resting upon the hair cells is a gelatinous membrane in which are embedded calcareous granules known as otoliths. Changes in linear acceleration alter the pressure of the otoliths, causing changes in the distortion of the cilia and providing an adequate stimulus for membrane depolarization. Within each macula the hair cells are arranged in two groups oriented in opposite directions, so that the receptor functions in a push-pull fashion within each organ. Since many of the nerve fibers passing from the hair cells to the brain are constantly active, this push-pull arrangement makes the receptors a highly sensitive detection system for linear acceleration in the vertical and horizontal planes.

Semicircular canals

The angular acceleration detectors within the semicircular canals function in a different way. The three canals—which in fact are considerably more than a semicircle in circumference—are oriented at approximately right angles to one another. Two are vertically placed, and one is at about 30 degrees to the horizontal. In this arrangement the anterior canal of one side of the head is in the plane of the posterior canal of the other side. A ridge, or crista, covered by sensory hair cells is located at the end of each canal within an expanded chamber called the ampulla. The canals are filled with an endolymphatic fluid. Rotation of the canals about an axis passing through the centre of each semicircle causes the fluid to flow toward or away from the crista, generating a force that bends the cilia by displacement of a gelatinous plate resting upon the hairs. The cells of the vertical canals are oriented in such a way that centrifugal movement away from the cristae depolarizes the hair cell membranes, while the converse applies to the horizontal canal.

Nerve supply

As in the case of the utricle and saccule, some of the nerve fibers conveying information from the cells are constantly active. The hair cells receive nerve impulses from the brain (via efferent fibers) and send them to the central nervous system (via afferent fibers). Excitatory efferent fibers increase the sensitivity of the hair cells, while inhibitory fibers decrease sensitivity. This system gives the semicircular canals a plasticity that is essential to maintaining optimal activity under different environmental conditions—including such extraordinary states as the microgravity encountered in space travel.

The vestibular apparatus is supplied by neurons that make up the vestibular portion of the vestibulocochlear, or eighth cranial, nerve. The somata, or cell bodies, of the afferent fibers lie in the vestibular ganglion near the end organ. Most of the nerve fibers pass from there to vestibular nuclei in the pons, while others pass directly to the cerebellum. The efferent fibers of the vestibular nerve arise from nuclei in the pons.

Vestibular functions

For vision to be effective, the retinal image must be stationary. This can be achieved only by maintaining the position of the eyes relative to the earth and using this stable platform for pursuing a moving target. The vestibular system plays a critical part in this, mainly through complex and incompletely understood connections between the vestibular apparatus and the musculature. Rotation of the head in any direction is detected by the semicircular canals, and a velocity signal is then passed via the vestibular nuclei to the somatic and extraocular muscles. In the case of the eye muscles, the velocity signal reaching the brain stem is in some way integrated with impulses signaling the eyes' position, thus ensuring that the eyes maintain their position relative to space and the object of regard. This integration partly occurs in the vestibular nuclei, the source of secondary neurons destined for the extraocular muscle nuclei of both sides.

Vestibulo-ocular reflex

When the head is oscillated, the eyes maintain their position in space but move in relation to the head. This so-called vestibulo-ocular reflex operates in both horizontal and vertical planes, owing to the arrangement of the three semicircular canals, and it maintains such stability that the object of vision does not oscillate until quite high velocities are attained. The other component of the vestibular system, the saccule and utricle, also contributes to the vestibulo-ocular reflex. Under normal circumstances the otolith receptors cause torsional movement of the eyes. For example, tilting the head toward one shoulder results in counter-rolling of the eyes, thereby stabilizing the image upon the retina. The two components of the vestibulo-ocular reflex also interact, enabling appropriate eye movements to be generated when both linear and angular accelerations are changing.

While the vestibulo-ocular reflex is the best understood of the vestibulo-motor connections, information from the vestibular receptors is also known to be passed via vestibular and other brain-stem nuclei to the somatic musculature of the trunk and limbs. Through these pathways body posture is adjusted to counter acceleration forces applied to the vestibule. These reflexes are so important in maintaining vertical posture that devastating short-term consequences on posture are seen if the vestibulocochlear nerve is cut.

Conscious sensation

Besides maintaining input for the generation of motor reflexes, vestibular impulses reach consciousness and create a powerful sensation. A person being rotated knows when he is accelerating even in the absence of an object upon which he can fix his eyes. This occurs because acceleration is the adequate stimulus for the semicircular canals. Similarly, information detected by the otoliths is readily brought to consciousness—as occurs, for example, when a darkened elevator accelerates up or down. The pathways to the cerebral cortex, which mediate conscious sensation, are not fully known, but there is considerable evidence that areas of the parietal and temporal lobes receive connections via the thalamus.

One important aspect of vestibular physiology is the interaction of vestibular impulses, which signal changes of position, and impulses from other sensory receptors that signal changes in bodily movement. For example, when the head turns to one side about a vertical axis, not only is the horizontal canal of that side stimulated and that of the other side inhibited, but receptors in the neck joints and muscles are also stimulated, and the retina indicates movement if fixation is not maintained perfectly. This information is fed to the brain via sensory pathways in the spinal cord and various visual sensory systems. Therefore, within the vestibular nuclei of the pons, neurons that respond to acceleration signals from the semicircular canals receive impulses from other sources as well. Other information from visual and spinal sensory systems pass to the cerebellum, which also receives direct impulses from the vestibular apparatus that bypass the vestibular nuclei. In this way the cerebellum has the opportunity to compare signals and assess the degree of mismatch between them. (Such mismatch is an unpleasant experience and is important in the phenomenon of motion sickness. Motion sickness is often generated by a mismatch between the various inputs signaling orientation within space. People will frequently be seasick if they are below decks in rough weather and the visual system signals no movement while the vestibular system indicates motion.) In another example, the vestibulo-ocular reflex may be underactive, so that for a given head movement the eyes do not deviate sufficiently within the orbit and the object of regard does not remain stationary upon the retina. Thus, the image slips and cannot be seen clearly during movement. The cerebellum has the opportunity to detect this mismatch between the required position of the eyes with respect to the environment and the movement actually achieved. Through inhibitory connections to the vestibular nuclei, the cerebellum can then adjust the vestibulo-ocular reflex so that a more appropriate movement of the eyes is achieved with the next acceleration signal. In other words, there is a continual updating of the vestibulo-ocular reflex via the cerebellum or structures associated with it.

A similar situation also obtains for somatosensory input from the spinal cord. A dramatic demonstration of short-term adaptation via the visual system occurs when someone dons prisms that reverse the perception of the environment in the horizontal plane, making everything look upside down. The person is at first unable to move about because any rotation of the head results in apparent movement of the environment in the wrong direction. However, over a few days normal mobility gradually returns. Incredibly, during this time the vestibulo-ocular reflex is at first diminished in amplitude and then is reversed. Removal of the prisms results in a rapid return to the normal state. These experiments are a powerful demonstration of the plasticity of the vestibulo-ocular reflex, which can continue functioning throughout life in spite of the various insults that befall it.

The eye

In order for the eye to function properly, specific autonomic functions must maintain adjustment of four types of smooth muscle: (1) smooth muscle of the iris, which controls the amount of light that passes through the pupil to the retina; (2) ciliary muscle on the inner aspect of the eye, which controls the ability to focus vision on nearby objects; (3) smooth muscle of arteries providing oxygen to the eye; and (4) the smooth muscle of veins that drain blood from the eye and affect intraocular pressure. In addition, the cornea must be kept moist by adequate secretion from the lacrimal gland.

Light reflex

When bright light is shined into an eye, the pupils of both eyes constrict. This response, termed the light reflex, is regulated by three structures: the retina, pretectum, and midbrain. In the retina is a three-neuron circuit consisting of light-sensitive photoreceptors (rods), bipolar cells, and retinal ganglion cells. The latter transmit luminosity information to the pretectum, where particular types of neurons relay the information to parasympathetic preganglionic neurons located in the Edinger-Westphal nucleus of the midbrain. These neurons send axons out of the ventral surface of the midbrain to synapse in the ciliary ganglion. From there, parasympathetic postganglionic neurons innervate the pupillary sphincter muscle, causing constriction.

Accommodation

In order to bring a nearby object into focus, several changes must occur in both the external and internal muscles of the eyes. The initial stimulus for accommodation is a blurred visual image that first reaches the visual cortex. From there, through a series of cortical connections, it reaches two specialized motor centres. One of these, located in the frontal cortex, sends motor commands to neurons in the oculomotor nucleus controlling the medial rectus muscles; this causes the eyes to converge. The other motor centre, located in the temporal lobe, functions as the accommodation area. Via multineuronal pathways, it activates specific parasympathetic pathways arising from the ciliary ganglion. This pathway causes the ciliary muscle to contract, thereby reducing tension on the lens and allowing it to become more rounded so the visual image of the near object can be focused on the central part of the retina. Concomitant with this change is a constriction of the iris, also under control of the oculomotor parasympathetic system, that acts to enhance the resolution of the lens.

The urinary system

The kidney is involved in maintenance of water and electrolyte balance. It also produces vasoactive hormones such as renin, a proteolytic enzyme that initiates the formation of angiotensin II (a potent hormone involved in the regulation of blood pressure), and erythropoietin, a glycoprotein hormone important in formation of red blood cells. While the autonomic nervous system is not crucial to these functions, the fine-tuning of some of these processes is regulated by sympathetic fibers. There is no known parasympathetic innervation of the kidney.

In contrast to renal functions, the normal physiology of the urinary bladder depends entirely on the autonomic nervous system. For example, retention of urine is made possible by activation of sympathetic pathways originating from lateral horns in spinal segments T11–L2; these cause contraction of smooth muscle that forms the internal urinary sphincter. Working in concert with this sphincter is the external urinary sphincter, which is made up of skeletal muscle controlled by motor fibers of the pudendal nerve. These fibers, arising from ventral horns of segments S2–S4, provide tonic excitation of the external sphincter. Because they are under voluntary control, micturition is initiated by higher brain centres. The first command causes voluntary inhibition of the sacral motor outflow, resulting in relaxation of the external urinary sphincter. Simultaneously, an increase in abdominal pressure, caused by contraction of muscles of the abdominal wall, starts an initial flow of urine. This is followed by a reflex inhibition of sympathetic outflow, resulting in relaxation of the internal urinary sphincter, and by activation of parasympathetic outflow to smooth muscle that causes the bladder to contract and expel the urine.

Sexual functions

The sexual response in both males and females can be defined by three physiological events. The first stage begins with psychogenic events in higher neural centres, which travel through multineuronal pathways and cause excitation of sacral parasympathetic outflow innervating vascular tissues of the penis and clitoris. This results in dilation of these arteries and erection of the penis and clitoris. The second stage involves secretion of glandular fluids; this is mediated by sympathetic neurons arising in the T12–L2 levels of the lateral horns. In the male, it involves contraction of the epididymis, vas deferens, seminal vesicles, and prostate gland, with the overall effect of moving fluids into the urethra; at the same time, sympathetic activation causes a closure of the internal urinary sphincter to prevent retrograde ejaculation of semen into the bladder. In the female, the response involves mucous secretions of the greater vestibular glands, resulting in lubrication of the vaginal orifice.

The third phase is a muscular response. Somatic efferent fibers in the pudendal nerve produce rhythmic contractions of the bulbocavernous and ischiocavernosus muscles in the male; this produces ejaculation. In the female, homologous muscles of the pelvic floor undergo rhythmic contractions controlled by somatic efferent neurons from the S2–S4 ventral horns.

The adrenal glands

The adrenal glands lie above the kidney and are therefore sometimes referred to by the older term suprarenal glands. They have a cortex and a medulla. The former synthesizes and secretes steroid hormones that are essential for life, but it is not under autonomic control. The adrenal medulla, on the other hand, is innervated by sympathetic preganglionic neurons. Within the adrenal medulla are chromaffin cells, which are homologous to sympathetic neurons and, like sympathetic neurons, are developed from embryonic neural crest cells. Chromaffin cells produce epinephrine (adrenalin) and, to a much lesser extent, norepinephrine as well as other chemicals such as chromogranins, enkephalins, and neuropeptide Y—all of which are released into the bloodstream and act as hormones. Epinephrine, in particular, affects many different types of tissues throughout the body and has a particularly potent effect on cells that possess b -adrenergic receptors.

The release of epinephrine prevents hypoglycemia (low blood sugar), through the following mechanism. By binding to a 2-adrenergic receptors embedded in the hormone-releasing cells of the pancreas, epinephrine inhibits the release of insulin. Since insulin promotes the absorption of glucose from the bloodstream into liver, skeletal muscle, and fat cells, inhibition of its release results in a greater amount of glucose that is available for entry into the brain. In addition, by binding to certain b -adrenergic receptors, epinephrine stimulates the release of glucagon, a pancreatic peptide hormone that acts in the liver to convert glycogen to glucose. Under emergency conditions, epinephrine causes even more widespread effects on glucose metabolism. Glycogen in the liver and skeletal muscle is broken down to glucose, fat held in adipose cells is converted to fatty acids and glycerol, and production of glucose and ketone bodies ( b -hydroxybutyric acid, acetoacetic acid) is increased in the liver. All these substances can be used as energy sources for the body.

The cardiovascular system

The function of the cardiovascular system is to maintain an adequate supply of oxygen to all tissues of the body. In order to maintain this function, the autonomic system must process visceral information and coordinate neural elements that innervate the heart, blood vessels, and respiration. In addition, certain hormones such as angiotensin II and vasopressin are released and act in concert with the autonomic nervous system.

The cardiovascular system

Reflex pathways

The cardiovascular system is regulated by sets of neurons that form two major types of reflex circuit. One type is triggered by mechanoreceptors found in the major arteries near the heart and in the heart itself. Lying in the wall of the aortic arch and the carotid sinuses are receptors sensitive to high pressure. These are innervated by the aortic branch of the vagus nerve and by a branch of the glossopharyngeal nerve. Both branches send information regarding increases in arterial blood pressure into the medulla oblongata and synapse in the nucleus of the solitary tract. Another group of mechanoreceptors provides information about venous pressure and volume; these are low-pressure receptors located in the walls of the major veins as they enter the heart and within the walls of the atria. Low-pressure afferents also relay sensory information to the solitary tract.

The mechanoreceptors described above trigger what is called the baroreceptor reflex, which causes a decrease in the discharge of sympathetic vasomotor and cardiac outflows whenever an increase in blood pressure occurs. In addition, the baroreceptor reflex causes stimulation of vagal cardioinhibitory neurons, which produces a decrease in heart rate, a decrease in cardiac contractility, and dilation of peripheral blood vessels. Overall, the net effect is to lower blood pressure.

The second major class of afferents that trigger reflex responses are chemoreceptors found in the major arteries near the heart in loci close to the high-pressure mechanoreceptors. Functioning as oxygen sensors, these receptors are innervated by separate sets of fibers that travel parallel with the baroreceptor nerves, and they also project to the nucleus of the solitary tract. Overall, the chemoreceptor reflex regulates respiration, cardiac output, and regional blood flow, ensuring that proper amounts of oxygen are delivered to the brain and heart.

Vasopressin and cardiovascular regulation

Vasopressin is a peptide hormone that is synthesized in magnocellular neurons of the supraoptic and paraventricular nuclei of the hypothalamus. These neurons send their axons into the posterior lobe of the pituitary gland, from which vasopressin is released into nearby capillaries and distributed throughout the body.

Vasopressin has two main functions: volume regulation and vasomotor tone. It acts to increase water retention by increasing the permeability of kidney tubules to water as the kidney filters blood plasma. As more water is reabsorbed, extracellular fluid volume is increased, and this in turn increases venous volume and, ultimately, blood pressure. Under emergency conditions, vasopressin also selectively constricts certain vascular beds that are nonessential for life (e.g., gastrointestinal, muscle); this shunts blood to critical tissues such as the heart or brain.

Two major stimuli trigger the release of this hormone: increases in extracellular fluid osmolality and decreases in blood volume (as in hemorrhage). Osmotic stimuli cause vasopressin to be released by acting on specialized brain centres called circumventricular organs. Surrounding the third and fourth ventricles of the brain and containing neurons with central projections that alter autonomic and neuroendocrine functions, these “osmosensitive” areas possess a unique vascular system that permits diffusion of large molecules such as peptides and ions to cross readily from the plasma to the brain. Normally, such chemical agents do not have free passage because the capillaries form a blood-brain barrier, but at these special sites they have direct access to central neurons. One of the areas, called the organum vasculosum of the lamina terminalis, lies in the third ventricle and is involved in osmo- and sodium regulation. Another circumventricular organ, called the subfornical organ, lies in the dorsal part of the third ventricle; it is particularly sensitive to hormones such as angiotensin II and signals changes needed for the regulation of salt and water balance. Both regions project directly to vasopressin-producing hypothalamic neurons. The area postrema, which lies on the floor of the fourth ventricle in the medulla, is the third site involved as a special chemical sensor of the plasma.

When blood is lost through hemorrhage, atrial receptors and baroreceptors relay volume and pressure information, via the vagus nerve, into the nucleus of the solitary tract. Neurons in this nucleus send commands to other relay neurons that project directly to the magnocellular hypothalamic neurons and cause the release of vasopressin.

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