CHOLINOCEPTIVE SITES IN DENERVATED SYMPATHETIC GANGLIA

¹ Department of Pharmacology, Schools of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

The responses to acetylcholine (ACh) of the superior cervical ganglia denervated for 6 to 70 days were compared with those of normal ganglia. The postganglionic firing evoked by ACh before and after the administration of eserine was the same essentially in ganglia denervated for 6 to 13 days as that evoked by ACh in normal ganglia. In both types of ganglia, the response to ACh consisted of a single component prior to the administration of eserine and of two components after treatment of the ganglia with eserine. Unlike normal ganghia, the responses to small doses of ACh of untreated ganglia which were denervated for 14 to 28 days were characterized by two components. The response to ACh of 6 out of 8 ganglia denervated for 30 to 70 days consisted of a single component. Treatment with eserine of these ganglia unmasked the bimodal response to ACh. Doses of eserine which failed to evoke directly postganglionic firing in ganglia denervated for shorter periods of time, produced a prolonged postganglionic discharge in the ganglia denervated longer than 30 days. As reported previously for normal ganghia, the eserine-induced discharge was blocked by small doses of atropine.

In all types of ganglia in which the bimodal response to ACh was demonstrated, the first component of the response was blocked by either d-tubocurarine or hexamethonium and the second component, by small doses of atropine. Similarly, repeated administration of potassium chloride unmasked the second component of the post-ganglionic response to injected ACh.

These findings support the concept of pharmacological heterogeneity of ganglionic cholinoceptive sites. The possibility is considered that some of the cholinoceptive sites are located on extrajunctional portions of the membrane of the ganglion cells. The unmasking by eserine, surgical denervation, and potassium ions of the cholinoceptive sites which are sensitive to blockade by atropine is discussed against the background of alterations in ganglionic electrolyte balance and alterations in membrane potentials.

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