• Jitendra N Singh, Gaurav Jain, Poduri Ramarao, and Shyam S Sharma.
• Electrophysiology Laboratory, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S. A. S. Nagar (Mohali) - 160 062. jnsingh@niper.ac.in
• Indian J. Physiol. Pharmacol. 2009 Apr 1;53(2):147-54.

AbstractCarbamazepine (CBZ), one of the most commonly prescribed antiepileptic drug, is proposed to inhibit Na+ channel. In this study, we have investigated the effects of CBZ on Na+ current, evoked in cultured dorsal root ganglion (DRG) neurons from neonatal rats using whole cell patch clamp technique. In small DRG neurons (20-25 microm), Na+ current was obtained by blocking K+ and Ca2+ currents with appropriate ion replacement and channel blockers. Separation of the Na+ current components was achieved on the basis of response to the conditioning voltage. The CBZ depressed Na+ current in a dose-dependent manner. The maximal Na+ current was depressed at 300 microM of CBZ, where 94 +/- 5.1% of depression was observed. The depression of normalized current amplitude was found to be 72 +/- 13.2%, 84 +/- 10%, 85 +/- 7.1% and 95 +/- 5.2% at 10, 30, 100 and 300 microM of CBZ concentrations, respectively, at -20 mV test pulse, when compared with control. The depression of current amplitude was observed as 48 +/- 12.3%, 42 +/- 15.2%, 71 +/- 17.7% and 90 +/- 5.8% at 10, 30, 100 and 300 microM of CBZ concentration, respectively, at 0 mV voltage pulse. The depression of Na+ currents was found to be dose-dependant at -20 and -10 mV but not at 0 mV, It is concluded that the depression of Na+ currents by CBZ may be responsible for inhibiting the neurotransmitter release.

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