CarbamazepineS1693

Carbamazepine inhibits the binding of [³H]batrachotoxinin A 20-α-benzoate (BTX-B) to a receptor site of voltage-sensitive sodium channel with IC50 of 131 μM, to decrease the activation of sodium channel ion flux in rat brain synaptosomes. Carbamazepine reduces receptor affinity due to an increased rate of ligand dissociation from the receptor-ligand complex, without altering maximal binding capacity from the scatchard analysis of BTX-B binding to synaptosome, suggesting an indirect allosteric mechanism for anticonvulsant inhibition of BTX-B binding. Carbamazepine does not alter basal ¹²⁵I-labeled scorpion toxin binding to synaptosomes in the absence of batrachotoxin, but when batrachotoxin (1.25 μM) added, Carbamazepine inhibits the batrachotoxin-dependent increase in scorpion toxin binding in a concentration-dependent manner with IC50 of 260 μM mediated at the alkaloid toxin binding site, none of which affects [³H]saxitoxin binding. ^[