Carbamazepine, a sodium channel blocker, is an anticonvulsant drug.Target: Sodium channelCarbamazepine 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 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 [1]. Carbamazepine at 25 mg/kg significantly increases extracellular levels of striatal and hippocampal dopamine (DA), 3,4-dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in a dose dependent manner, while Carbamazepine at 50 mg/kg significantly decreases total levels of striatal DA and DOPA as well as hippocampal HVA, but has no effect on total levels of striatal DOPAC and HVA nor on hippocampal DA, DOPA and DOPAC [2].

References:
[1]. Willow, M. and W.A. Catterall, Inhibition of binding of [3H]batrachotoxinin A 20-alpha-benzoate to sodium channels by the anticonvulsant drugs diphenylhydantoin and carbamazepine. Mol Pharmacol, 1982. 22(3): p. 627-35.
[2]. Okada, M., et al., Biphasic effects of carbamazepine on the dopaminergic system in rat striatum and hippocampus. Epilepsy Res, 1997. 28(2): p. 143-53.