Abstract

Intracellular recordings from goldfish auditory afferents revealed a hyperpolarization triggered by a single impulse in the Mauthner cell. The firing of either one of the two Mauthner cells alone was sufficient to evoke this potential change. The all or none hyperpolarization, which could only be recorded in some auditory fibers, presumably was an inhibitory postsynaptic potential. The inhibitory postsynaptic potential typically had a latency of 6 ms, an amplitude of 1 mV and a half-decay time of 6.8 ms; it could block or delay impulses evoked by direct current injection and could attenuate the amplitude of excitatory postsynaptic potentials evoked by sound pulses. However, this inhibitory postsynaptic potential did not reduce the amplitudes of electrotonic coupling potentials produced by antidromic impulses in the Mauthner cell. We propose that the inhibitory postsynaptic potential is generated at the dendrites of the auditory fibers, i.e. in the ear, rather than at the central terminals of the afferent, where the antidromic coupling potentials originate. The possibility that the inhibitory postsynaptic potential actually represented disfacilitation due to an efferent inhibition of the hair cells, which tonically depolarize the saccular fibers, was ruled out because depolarization of these fibers increased the inhibitory postsynaptic potential amplitude. Possible morphological substrates for the efferent inhibition and the behavioral significance of this inhibition are discussed.

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