ALTERATIONS OF TRANSMISSION IN SYMPATHETIC GANGLIA TREATED WITH A SULFHYDRYL-GROUP INHIBITOR, N-ETHYLMALEIMIDE (NEM)

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

N-Ethylmaleimide (NEM) produced a series of changes in the responses of the superior cervical ganglion to stimulation of the preganglionic nerve and injected ganglionic stimulating drugs. On the basis of the time-courses of the changes, these alterations could be grouped into three divisions: viz., immediate, late, and delayed. The immediate change in ganglionic function produced by NEM was an enhancement of the postganglionic spike and a depression of the responses evoked by acetylcholine (ACh), potassium chloride (KCl), or tetramethylammonium ions (TMA). The responses of denervated ganglia to these agents were blocked also by NEM. Conversely, the late change produced by NEM consisted of an enhancement of the responses of the ganglia to the ganglionic stimulants at a time when the response to stimulation of the preganglionic nerve was depressed or even abolished. A similar late change was produced in the responses of denervated ganglia to the stimulating drugs. Furthermore, retrograde firing along the preganglionic nerve evoked by KCl was enhanced by NEM. The delayed change in ganglionic activity was the occurrence of spontaneous pre- and postganglionic asynchronous discharges. The asynchronous firing of the postganglionic nerve was not affected by atropine, hexamethonium, or mecamylamine; was enhanced by d-tubocurarine and tetraethylammonium; and was blocked by calcium chloride and magnesium chloride. Hexamethonium blocked the excitatory action of d-tubocurarine. The preganglionic firing, although blocked by calcium ions, was not affected by any of the ganglionic blocking agents.

These findings are compared with the changes in ganglionic activity which occur in sympathetic ganglia deprived of calcium ions.