An effect of diphenylhydantoin on posttetanic hyperpolarization of intramedullary nerve terminals.

Diphenythydantoin (DPH), in anticonvulsant doses, abolishes posttetanic hyperpolarization originating in the central terminals of dorsal root fibers of spinal cats. Depression of posttetanic hyperpolarization by DPH probably accounts for the drug9s reduction of posttetanic potentiation in the monosynaptic reflex and repetitive afterdischarges originating in nerve terminal structures. Since the latter two phenomena have been implicated as possible seizure mechanisms, depression of posttetanic hyperpolarization may be a more fundamental anticonvulsant property.