Abstract
ElectrophysiologicaI studies were performed to elucidate the mechanism underlying the antivertigo action of eperisone, an antispastic drug, using cats anesthetized with α-chloralose. lontophoretic application of eperisone up to 100 nA produced a dose-dependent inhibition of spike generation upon vestibular nerve stimulation in monosynaptic and polysynaptic neurons of the medial vestibular nucleus (MVN). The inhibition of neurons in the MVN was more prominent than that in the lateral vestibular nucleus. In addition, iontophoretically applied eperisone in doses of 50-100 nA inhibited the orthodromic spike elicited by vestibular nerve stimulation in the MVN monosynaptic neurons projecting to the abducens nucleus (ascending neuron), without affecting that in the MVN neurons projecting to the spinal cord (descending neuron). An inhibition of antidromic spike elicited by abducens nucleus stimulation in the MVN monosynaptic ascending neurons was observed in some cases during application of eperisone. These results suggest that eperisone predominantly inhibits synaptic transmission of the MVN ascending neurons.
