Autonomic ganglia have been the subject of interest for many years in the study of interactions between drugs and nervous tissues. The first important account84 was given by Langley and described the stimulating and blocking actions of nicotine on sympathetic ganglia. It was found that small amounts of nicotine stimulated ganglia and then produced a blockade of ganglionic transmission because of persistent depolarization. From these experiments, Langley was able to outline the general pattern of innervation of organs by the autonomic nervous system. Parasympathetic ganglia usually are located near the organ they innervate and have preganglionic fibers that stem from the cervical and thoracic regions of the spinal cord. Sympathetic ganglia consist of 22 pairs that lie on either side of the vertebral column to form lateral chains. These ganglia are connected both to each other by nerve trunks and to the lumbar or sacral regions of the spinal cord.
Using the sympathetic cervical ganglion as a model revealed that transmission in the autonomic ganglion is more complex than formerly believed. Traditionally, stimulation of autonomic ganglia by ACh was considered to be the nicotinic action of the neurotransmitter. It is now understood that stimulation by ACh produces a triphasic response in sympathetic ganglia. Impulse transmission through the ganglion occurs when ACh is released from preganglionic fibers and activates the N2 nicotinic receptors of the neuronal membrane. This triggers an increase in sodium and potassium conductances of a subsynaptic membrane, resulting in an initial excitatory postsynaptic potential (EPSP) with a latency of 1 ms, followed by an inhibitory postsynaptic potential (IPSP) with a latency of 35 ms, and, finally, a slowly generating EPSP with a latency of several hundred milliseconds. The ACh released by preganglionic fibers also activates M1 muscarinic receptors of the ganglion and probably of the small-intensity fluorescent (SIF) cell. This results in the appearance of a slow IPSP and a slow EPSP in the neurons of the ganglion.85 The initial EPSP is blocked by conventional competitive nondepolarizing ganglionic blocking agents, such as hexamethonium, and is considered the primary
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