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Lamotrigine is an antiepileptic drug widely used to treat epileptic seizures. Using whole-cell voltage clamp recordings in combination with a fast drug application approach, we investigated the effects of lamotrigine on 5-hydroxytryptamine (5-HT) 3 receptors in NCB-20 neuroblastoma cells. Co-application of lamotrigine (1~300 µM) resulted in a concentration-dependent reduction in peak amplitude of currents induced by 3 µM of 5-HT for an IC 50 value of 28.2±3.6 µM with a Hill coefficient of 1.2±0.1. These peak amplitude decreases were accompanied by the rise slope reduction. In addition, 5-HT 3 -mediated currents evoked by 1 mM dopamine, a partial 5-HT 3 receptor agonist, were inhibited by lamotrigine co-application. The EC 50 of 5-HT for 5-HT 3 receptor currents were shifted to the right by co-application of lamotrigine without a significant change of maximal effect. Currents activated by 5-HT and lamotrigine co-application in the presence of 1 min pretreatment of lamotrigine were similar to those activated by 5-HT and lamotrigine co-application alone. Moreover, subsequent application of lamotrigine in the presence of 5-HT and 5-hydroxyindole, known to attenuate 5-HT 3 receptor desensitization, inhibited 5-HT 3 receptor currents in a concentration-dependent manner. The deactivation of 5-HT 3 receptor was delayed by washing with an external solution containing lamotrigine. Lamotrigine accelerated the desensitization process of 5-HT 3 receptors. There was no voltage-dependency in the inhibitory effects of lamotrigine on the 5-HT 3 receptor currents. These results indicate that lamotrigine inhibits 5-HT 3 -activated currents in a competitive manner by binding to the open state of the channels and blocking channel activation or accelerating receptor desensitization.

Lamotrigine, an antiepileptic drug, inhibits 5-HT3receptor currents in NCB-20 neuroblastoma cells

Lamotrigine, an antiepileptic drug, inhibits 5-HT₃receptor currents in NCB-20 neuroblastoma cells