Studies on the synaptic facilitatory action of nikethamide

Abstract

In spinal unanaesthetized cats, intravenously administered nikethamide (12–100 mg/kg) promptly increased the size of monosynaptic and polysynaptic responses without altering the amplitude or latency of the afferent volley. Furthermore, it depressed the dorsal root potential but facilitated the dorsal root reflex and increased spontaneous ventral root discharges. No consistent changes in presynaptic or postsynaptic inhibition were observed. Repeated administration of equal doses of nikethamide produced no decrement in facilitation of monosynaptic transmission. Paired monosynaptic responses evoked by maximal double dorsal root stimuli separated by 400 msec-intervals were equally facilitated. In lower doses that did not produce pronounced blood pressure alterations, nikethamide produced no changes in the direct excitability of motoneuronal somas or of presynaptie terminals. It is also shown that nikethamide effectively antagonizes the depression of spinal monosynaptic transmission induced by pentobarbital, but antagonism of the depression of polysynaptic transmission is incomplete. Possible mechanisms whereby nikethamide may exert its facilitatory effects are discussed.