Abstract

The present study examined transmitters that regulate commissural inhibition. Extracellular spikes of a single vestibular neuron were recorded in decerebrated cats. Multibarreled electrodes were filled with transmitter candidates (GABA and glycine), their specific antagonists (bicuculline, strychnine) and 2 M NaCl for extracellular recording. After isolation of a type I neuron, chemicals were iontophoretically applied to examine their effects on the activity of the neuron. The results were as follows. Commissural inhibition caused by electrical stimulation of the contralateral labyrinth was not abolished by the application of strychnine (a glycine antagonist), but was abolished by bicuculline (a GABA antagonist). Commissural inhibition was not abolished by phaclofen. Some bicuculline-sensitive neurons, with a short-latency commissural inhibition (presumably disynaptic inhibition), showed spacial summation when the conditioning stimulation (contralateral vestibular nerve stimulation) was applied with the test stimulation (vestibular nucleus stimulation). It was concluded that commissural inhibition was activated by the GABAA receptor, but not by the GABAB receptor, that the inhibitory type I neurons located in the contralateral vestibular nucleus were GABAergic, and that inhibitory type II neurons were also GABAergic neurons.

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