Spontaneous impulses are discharged simultaneously and synchronously in pre-and post-ganglionic nerves of rat sympathetic ganglia infected with pseudo-rabies virus (Dempsher, Larrabee, Bang & Bodian, 1955). The virusinduced activity in the preganglionic nerve is antidromic (in a direction opposite to that occurring normally), whereas in the post-ganglionic nerve the activity is orthodromic or in the normal direction. In order to explain this derangement, the assumption was made that the activity had its origin in the preganglionic nerve endings and was produced by spontaneously released acetylcholine (ACh) acting upon the preganglionic nerve endings made superirritable by the virus infection (Dempsher & Riker, 1957). In support of this assumption were the following observations. Failure of virus-induced activity to develop in ganglia infected after preganglionic denervation, and the presence of spontaneous impulses in the preganglionic nerve in advanced infections whenever electrical stimulation failed to evoke a post-ganglionic response, supported the view that the site of origin (pace-maker) of the activity was located in the presynaptic nerve. Suppression of spontaneous impulses in the preganglionic nerve whenever that nerve was deprived of its endings, and suppression of activity occurring only in the post-ganglionic nerve by removal of calcium from the bathing solution, were interpreted to mean that the pace-maker was located in the presynaptic nerve endings. The simultaneous and synchronous increase in activity in both nerves produced by physostigmine, and the simultaneous and synchronous decrease in activity in both nerves whenever tubocurarine was applied, supported the view that the virus-induced activity was caused by ACh, and the site of action of ACh was the pace-maker located in the presynaptic nerve endings. In accord with this interpretation were the following observations. Applied ACh produced a simultaneous and synchronous increase in activity in both nerves, thus
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