The mechanism of action of the anticonvulsant drug carbamazepine was studied in rat hippocampal and amygdaloid slices using intracellular recording techniques. Stimulation of the Schaffer collateral/commissural pathway evoked an excitatory postsynaptic potential (EPSP) in CA1 pyramidal cells. Thirty minutes after superfusing with Mg ++ -free solution, the same stimulus intensity triggered burst firing. Application of carbamazepine reversibly reduced the burst duration in a dose-dependent manner. Synaptic response mediated by the N-methyl-D-aspartate (NMDA) receptors (EPSP(NMDA)) was isolated pharmacologically by application of a solution containing non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX,10 μM) and γ-aminobutyric acid(A) recept or antagonist picrotoxin (50 μM). Carbamazepine reversibly blocked the amplitude of EPSP(NMDA) in a concentration which did not affect the normal synaptic transmission. These results suggest that the combined blockade of NMDA receptors and firing of action potential forms the basis for the anticonvulsant effect of carbamazepine.
|頁（從 - 到）||199-204|
|期刊||Chinese Journal of Physiology|
|出版狀態||Published - 1993|
All Science Journal Classification (ASJC) codes
- Physiology (medical)