The activities of the GI tract are controlled locally through a restricted part of the peripheral nervous system called the enteric nervous system (ENS). The ENS is involved in sensorimotor control and consists of both afferent sensory neurons and a number of motor nerves and interneurons that are organized principally into two nerve plexuses: the myenteric (Auerbach's) plexus and the submucosal (Meissner's) plexus. The myenteric plexus, located between the longitudinal and circular muscle layers, plays an important role in the contraction and relaxation of GI smooth muscle. The submucosal plexus is involved with secretory and absorptive functions of the GI epithelium, local blood flow, and neuroimmune activities. The ENS consists of components of the sympathetic and parasympathetic branches of the ANS and has sensory nerve connections through the spinal and nodose ganglia (see Chapter 37).
Parasympathetic input to the GI tract is excitatory; preganglionic neurons in the vagus innervate the parasympathetic ganglia of the enteric plexuses. Postganglionic sympathetic nerves also synapse with the intramural enteric parasympathetic ganglia. Sympathetic nerve activity induces relaxation primarily by inhibiting the release ofACh from the preganglionic fibers.
The intrinsic primary afferent neurons are present in both the myenteric and submucosal plexuses. They respond to luminal chemical stimuli, to mechanical deformation of the mucosa, and to stretch. The nerve endings of the primary afferent neurons can be activated by endogenous substances (e.g., serotonin) arising from local enterochromaffin cells or possibly from serotoner-gic nerves.
The muscle layers of the GI tract are dually innervated by excitatory and inhibitory motor neurons whose cell bodies are in the gut wall. ACh, in addition to being the transmitter of parasym-pathetic nerves to the ENS, is the primary excitatory transmitter acting on nicotinic acetylcholine receptors (nAChRs) in ascending intramural pathways. Pharmacological blockade of cholinergic neurotransmission, however, does not completely abolish this excitatory transmission because cotransmitters, such as substance P and neurokinin A, are coreleased with ACh and contribute to the excitatory response; similarly, ATP acts as an excitatory neurotransmitter via P2X receptors.
Inhibitory neurons of the ENS release a variety of transmitters and cotransmitters, including nitric oxide (NO), ATP (acting on P2Y receptors), VIP, and pituitary adenylyl cyclase—activating peptide (PACAP); NO is a primary inhibitory transmitter. Interstitial cells of Cajal (ICC) relay signals from the nerves to the smooth muscle cells to which they are electrically coupled. The ICC have receptors for both the inhibitory transmitter NO and the excitatory tachykinins. Disruption of the ICC impairs excitatory and inhibitory neurotransmission.
DIFFERENCES AMONGST SYMPATHETIC, PARASYMPATHETIC, AND MOTOR NERVES A preganglionic sympathetic fiber may traverse a considerable distance of the sympathetic chain and pass through several ganglia before it finally synapses with a postganglionic neuron; also, its terminals contact a large number of postganglionic neurons, and one ganglion cell may be supplied by several preganglionic fibers, such that the ratio of preganglionic axons to ganglion cells may be >1:20. This organization permits a diffuse discharge of the sympathetic system.
The parasympathetic system, in contrast, has terminal ganglia very near or within the organs innervated and thus is more circumscribed in its influences. In some organs, there is a 1:1 relationship between the number of preganglionic and postganglionic fibers (this distinction does not apply to all sites; in the myenteric plexus, this ratio is -1:8000).
The cell bodies of somatic motor neurons reside in the ventral horn of the spinal cord (see Figure 6-1); the axon divides into many branches, each of which innervates a single muscle fiber, so more than 100 muscle fibers may be supplied by one motor neuron to form a motor unit. At each neuromuscular junction, the axonal terminal loses its myelin sheath and forms a terminal arborization that lies in apposition to a specialized surface of the muscle membrane, the motor end plate (see Figure 9-2).
RESPONSES OF EFFECTOR ORGANS TO AUTONOMIC NERVE IMPULSES From the responses of the various effector organs to autonomic nerve impulses and the knowledge of the intrinsic autonomic tone, one can predict the actions of drugs that mimic or inhibit the actions of these nerves. In some instances, the sympathetic and parasympathetic neurotransmitters can be viewed as physiological or functional antagonists. Most viscera are innervated by both divisions of the ANS, and the level of activity at any moment represents the sum of influences of the two components. Effects of sympathetic and parasympathetic stimulation of the heart and the iris show a pattern of functional antagonism in controlling heart rate and pupillary aperture, respectively, whereas their actions on male sexual organs are complementary and are integrated to promote sexual function. The control of peripheral vascular resistance is due primarily, but not exclusively, to sympathetic control of the contraction of arteriolar smooth muscle. The effects of stimulating the sympathetic and parasympathetic nerves to various organs, visceral structures, and effector cells are summarized in Table 6-1.
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