Abstract
Current pharmacological concepts embrace the possibility that drugs acting at junctions, where acetylcholine plays an important though perhaps not essential rôle in transmission, do so by exerting their influence on some step in the cholinergic mechanism.
The consistency of such a view was examined by studying the effects on a sympathetic ganglion of drugs known to act at the parasympathetic neuro-effector junctions, since both are sites where cholinergic systems operate. Pertinent observations may be found in papers by Langley, 1 by Dale and Laidlaw, 2 etc.
Action potentials of the tonic impulses normally coursing in the superior cervical preganglionic trunk of the rabbit (anesthetized with nembutal) and of the response in the postganglionic fibers were recorded by a Matthews oscillograph after amplification. The waves were also spread out for visual observation by a rotating mirror (speed corresponding to 1.8 meters per second) and converted into sound by a loud speaker.
Pilocarpine, representing the parasympathomimetic stimulants, and atropine, the depressants, were injected into the common carotid artery, all branches except to the ganglion having been ligated and cut and the carotid sinus nerve severed. Thus the ganglionic circulation was retained intact while allowing an effective concentration at the synapse before diffusion into the general circulation. This made possible the observation of local effects uncomplicated by distant actions such as on the central nervous system directly, or indirectly through the remaining innervated carotid sinus responding to vascular changes.
The increase in postganglionic impulses (compare records A and B, C and D) illustrates the stimulant effect of small doses of pilocarpine. This increase, seen again in E, F, took place without any change in the corresponding preganglionic records G and H, and consequently must have been due to a truly peripheral action at the synapse.
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