Sunday, July 27, 2008

AnatomyPhysiology of ANS

Anatomy Physiology of Autonomic Nervous System
(Physiology from Ganong - Review Of Medical Physiology - 20th Ed)
(Anatomy from Lippincott Williams & Wilkins Atlas of Anatomy, 1st Edition. 2008 )

INTRODUCTION


The autonomic nervous system, like the somatic nervous system, is organized on the basis of the reflex arc. Impulses initiated in visceral receptors are relayed via afferent autonomic pathways to the CNS, integrated within it at various levels, and transmitted via efferent pathways to visceral effectors. This organization deserves emphasis because the functionally important afferent components have often been ignored. The efferent pathways to the viscera are the subject of this chapter.

Anatomically, the autonomic outflow is divided into two components: the sympathetic and parasympathetic divisions of the autonomic nervous system. In the gastrointestinal tract, these both communicate with the enteric nervous system, and this is sometimes called a third division of the autonomic nervous system.

Sympathetic Division

The axons of the sympathetic preganglionic neurons leave the spinal cord with the ventral roots of the first thoracic to the third or fourth lumbar spinal nerves. They pass via the white rami communicantes to the paravertebral sympathetic ganglion chain, where most of them end on the cell bodies of the postganglionic neurons. The axons of some of the postganglionic neurons pass to the viscera in the various sympathetic nerves. Others reenter the spinal nerves via the gray rami communicantes from the chain ganglia and are distributed to autonomic effectors in the areas supplied by these spinal nerves. The postganglionic sympathetic nerves to the head originate in the superior, middle, and stellate ganglia in the cranial extension of the sympathetic ganglion chain and travel to the effectors with the blood vessels. Some preganglionic neurons pass through the paravertebral ganglion chain and end on postganglionic neurons located in collateral ganglia close to the viscera. Parts of the uterus and the male genital tract are innervated by a special system of short noradrenergic neurons with cell bodies in ganglia in or near these organs, and the preganglionic fibers to these postganglionic neurons presumably go all the way to the organs. In addition, it has recently been demonstrated that at least in rats there are intrinsic cardiac adrenergic cells (ICA cells). These cells contain epinephrine and norepinephrine and account for about 15% of the total catecholamine content of the heart. Their exact function is unsettled, but gene knockout experiments indicate that catecholamines are essential for normal development of the heart.



Fig.1. Pathways of the Sympathetic Nervous System. (click image to enlarge)
Image from Lippincott Williams & Wilkins Atlas of Anatomy, 1st Edition. 2008

Parasympathetic Division

The cranial outflow of the parasympathetic division supplies the visceral structures in the head via the oculomotor, facial, and glossopharyngeal nerves, and those in the thorax and upper abdomen via the vagus nerves. The sacral outflow supplies the pelvic viscera via the pelvic branches of the second to fourth sacral spinal nerves. The preganglionic fibers in both outflows end on short postganglionic neurons located on or near the visceral structures
Fig.2. Pathways of the Parasympathetic Nervous System. (click image to enlarge)
Image from Lippincott Williams & Wilkins Atlas of Anatomy, 1st Edition. 2008

RESPONSES OF EFFECTOR ORGANS TO AUTONOMIC NERVE IMPULSES

General Principles

The effects of stimulation of the noradrenergic and cholinergic postganglionic nerve fibers to the viscera are listed in. The smooth muscle in the walls of the hollow viscera is generally innervated by both noradrenergic and cholinergic fibers, and activity in one of these systems increases the intrinsic activity of the smooth muscle whereas activity in the other decreases it. However, there is no uniform rule about which system stimulates and which inhibits. In the case of sphincter muscles, both noradrenergic and cholinergic innervations are excitatory, but one supplies the constrictor component of the sphincter and the other the dilator.

There is usually no acetylcholine in the circulating blood, and the effects of localized cholinergic discharge are generally discrete and of short duration because of the high concentration of acetylcholinesterase at cholinergic nerve endings. Norepinephrine spreads farther and has a more prolonged action than acetylcholine. Norepinephrine, epinephrine, and dopamine are all found in plasma. The epinephrine and some of the dopamine come from the adrenal medulla, but most of the norepinephrine diffuses into the bloodstream from noradrenergic nerve endings. Metabolites of norepinephrine and dopamine also enter the circulation, some from the sympathetic nerve endings and some from smooth muscle cells. It is worth noting that even when MAO and COMT are both inhibited, the metabolism of norepinephrine is still rapid. However, inhibition of reuptake prolongs its half-life.

Cholinergic Discharge

In a general way, the functions promoted by activity in the cholinergic division of the autonomic nervous system are those concerned with the vegetative aspects of day-to-day living. For example, cholinergic action favors digestion and absorption of food by increasing the activity of the intestinal musculature, increasing gastric secretion, and relaxing the pyloric sphincter. For this reason, and to contrast it with the "catabolic" noradrenergic division, the cholinergic division is sometimes called the anabolic nervous system.

The function of the VIP released from postganglionic cholinergic neurons is unsettled, but there is evidence that it facilitates the postsynaptic actions of acetylcholine. Since VIP is a vasodilator, it may also increase blood flow in target organs.

Noradrenergic Discharge

The noradrenergic division discharges as a unit in emergency situations. The effects of this discharge are of considerable value in preparing the individual to cope with the emergency, although it is important to avoid the teleologic fallacy involved in the statement that the system discharges in order to do this. For example, noradrenergic discharge relaxes accommodation and dilates the pupils (letting more light into the eyes), accelerates the heartbeat and raises the blood pressure (providing better perfusion of the vital organs and muscles), and constricts the blood vessels of the skin (which limits bleeding from wounds). Noradrenergic discharge also leads to lower thresholds in the reticular formation (reinforcing the alert, aroused state) and to elevated plasma glucose and free fatty acid levels (supplying more energy). On the basis of effects like these, Cannon called the emergency- induced discharge of the noradrenergic nervous system the "preparation for flight or fight."

The emphasis on mass discharge in stressful situations should not obscure the fact that the noradrenergic autonomic fibers also subserve other functions. For example, tonic noradrenergic discharge to the arterioles maintains arterial pressure, and variations in this tonic discharge are the mechanism by which carotid sinus feedback regulation of blood pressure is effected. In addition, sympathetic discharge is decreased in fasting animals and increased when fasted animals are refed. These changes may explain the decrease in blood pressure and metabolic rate produced by fasting and the opposite changes produced by feeding.

The small granulated vesicles in postganglionic noradrenergic neurons contain ATP and norepinephrine, and the large granulated vesicles contain neuropeptide Y. There is evidence that low-frequency stimulation promotes release of ATP whereas high-frequency stimulation causes release of neuropeptide Y. However, the functions of the released ATP and neuropeptide Y are unsettled.

Autonomic Pharmacology

The junctions in the peripheral autonomic motor pathways are a logical site for pharmacologic manipulation of visceral function because transmission across them is chemical. The transmitter agents are synthesized, stored in the nerve endings, and released near the neurons, muscle cells, or gland cells on which they act. They bind to receptors on these cells, thus initiating their characteristic actions, and they are then removed from the area by reuptake or metabolism. Each of these steps can be stimulated or inhibited, with predictable consequences. In noradrenergic endings, certain drugs also cause the formation of compounds that replace norepinephrine in the granules, and these weak or inactive "false transmitters" are released instead of norepinephrine by the action potentials reaching the endings.



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