The present study was aimed at elucidating the possible mechanisms und
erlying the anticonvulsant efficacy of phenytoin Sodium channel using
intracellular recording techniques in the in vitro amygdalar channel d
alar slice preparation. Synaptic response mediated by the N-methyl-D-a
spartate (NMDA) receptor (EPSPNMDA) was isolated pharmacologically by
application of a solution containing non-NMDA receptor antagonist 6-cy
ano-7-nitroquinoxaline-2,3-dione (10 mu mol/l) and gamma-aminobutyric
acid(A) receptor antagonist bicuculline (20 mu mol/l). Phenytoin inhib
its the amplitude of EPSPNMDA without affecting the postsynaptic depol
arization induced by exogenous application of NMDA, In addition, pheny
toin increases the magnitude of paired-pulse facilitation which is con
sistent with a presynaptic mode of action. These results suggest that
inhibition of transmitter release due to presynaptic blockade of Na+ a
nd/or Ca2+ channels may account largely for the anticonvulsant efficac
y of phenytoin.