Carbamazepine inhibits NMDA-induced depolarizations in cortical wedges prepared from DBA/2 mice.
There is some doubt as to the mechanism of action of the widely-used anticonvulsant drug, carbamazepine. In cortical wedges prepared from genetically epilepsy-prone DBA/2 mice, carbamazepine at therapeutic concentrations (1-10 microM) markedly reduced the depolarization produced by N-methyl-D-aspartate (NMDA). The NMDA sub-type of glutamate receptor has been implicated in the pathogenesis of epilepsy and the inhibitory action of carbamazepine on this response suggests that the anticonvulsant action of the drug may be due to its blockade of NMDA receptor-mediated events.
Lancaster
J M
JM
Department of Pharmacology and Therapeutics, University of Wales College of Medicine, Heath Park, Cardiff, Great Britain.
Davies
J A
JA
D000818:Animals; D002220:Carbamazepine / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004827:Epilepsy / Q000503:physiopathology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects*; D051379:Mice; D008811:Mice, Inbred DBA; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors*
D002220:Carbamazepine; D016202:N-Methylaspartate