A study of presynaptic slow potentials in virus‐infected sympathetic ganglia of the rat

Abstract

In order to explain the occurrence of spontaneous impulses, originating in presynaptic nerve endings and discharged simultaneously and synchronously in pre-and post-ganglionic nerves of rat sympathetic ganglia infected with pseudo-rabies virus, the following working hypothesis was adopted. Spontaneous impulses originated in presynaptic nerve endings because the virus infection interfered with the normal action of an inhibiting system having its origin in the central nervous system (c.N.s.) and exerting its action upon the presynaptic nerve endings through the release of substances such as gamma aminobutyric acid, adrenaline, and noradrenaline. Interference with the normal action of the inhibitory system resulted in a spontaneous release of acetylcholine (ACh), which stimulated the presynaptic nerve endings to initiate the discharge of impulses in both nerves, antidromic in the preganglionic nerve, orthodromic in the postganglionic nerve (Dempsher, Larrabee, Bang & Bodian, 1955;Dempsher & Riker, 1957;Dempsher, Tokumaru & Zabara, 1959).An inherent weakness of the working concept presented above has been that, although based on experiments in which we used electrophysiological techniques, no electrical event had been described which could actually be located in the presynaptic nerve endings, the suggested site of interaction of excitatory and inhibitory systems. The purpose of this paper is to report experiments supporting the suggestion that the electrical event in the presynaptic nerve endings accompanying interaction of excitatory and inhibitory systems in virus-infected rat sympathetic ganglia is a slowly changing, decreasing potential change, the presynaptic slow potential. METHODS Preparation of the virus inoculum to infect the rat superior cervical ganglion was described in detail in previous publications (Tokumaru, 1957;Dempsher et al. 1959). Briefly, rat superior cervical ganglia were infected following intraocular inoculations of 005 ml. of undiluted suspension of L strain pseudo-rabies virus harvested from infected 14 PHYSIO. CLI

A New General Concept of the Neurohumoral Functions of Acetylcholine and Acetylcholinesterase

“…Dempsher and his associates have shown that in the pathological condition resulting from infection with pseudorabies virus, spontaneous and synchronous postganglionic and antidromic preganglionic firing arises from the superior cervical ganglion (Dempsher and others, 1955), and that this is probably due to the action of ACh released from the presynaptic terminals (Dempsher and Riker, 1957). Furthermore, they have detected at both poles of such gangha slow waves of localised depolarisation, on which the propagated spikes are superimposed (Dempsher and Zabara, 1960) ; the former appear to represent typical generator potentials which have generally been thought to occur only at the postsynaptic side of the junction. It is possible that the mechanisms underlying these virusinduced phenomena are a combination of destruction of much of the presynaptic AChE, and extension centrally of the area of ACh-excitability of the axonal terminals, comparable to that which occurs distally at the sarcoplasmic membrane of skeletal muscle fibres after denervation (Axelsson and Thesleff, 1959).…”

Synaptic function in the nervous system: A theory and its application

“…Experimental. The experimental method has been described in detail elsewhere (Dempsher, Larrabee, Bang and Bodian, 1955;Dempsher, Tokumaru and Zabara, 1959;Dempsher and Zabara, 1960). Briefly, it is as follows:…”

A bio-physical basis of mathematics in synaptic function of the nervous system: A theory

“…However, it has also been clearly shown that curare blocks cholinergic sites in presynaptic terminals of sympathetic ganglia. (Dempsher and Riker, 1957;Dempsher and Zabara, 1960). The identity of the cholinergic receptor is not exactly known.…”