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