Abstract

ABSTRACT Ultrastructural studies have revealed input synapses on the central terminals of many sensory afferent neurones in both vertebrates (Maxwell et al. 1982; Ralston et al. 1984) and invertebrates (Altman et al. 1980; Watson and Pflüger, 1984). Indeed presynaptic modulation of sensory information flowing into the central nervous system appears to be a very widespread phenomenon. It may take the form of either inhibition (Eccles, 1964) or facilitation (Klein and Kandel, 1980), but it is the former that is most widely known from physiological experiments. Several mechanisms can bring about presynaptic inhibition. (1) Depolarization of an afferent terminal may reduce the amplitude of the action potential, leading to a reduction of the calcium influx and, consequently, of transmitter release (Miledi and Slater, 1966; Blagbum and Sattelle, 1987). (2) A conductance increase in the terminal may reduce the height of an action potential regardless of the direction of the potential change (Baxter and Bittner, 1981; Hue and Callec, 1983) and block spike conduction through small-diameter axonal branches (Atwood, 1976). The most widely suggested mechanism for this in both vertebrates (Nicholl and Alger, 1979) and invertebrates (Kennedy et al. 1980) is an increase in chloride conductance mediated by GABA. (3) The presynaptic calcium current may be reduced by the direct action of a neurotransmitter (Shapiro et al. 1980).

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