ABSTRACT
This chapter aims to integrate the information derived from in vitro experiments with what we have learned from in vivo studies in an effort to obtain as accurate as possible a picture of the mechanism of action of carbamazepine. Many of the antiepileptic drugs currently in use were discovered more or less fortuitously, and carbamazepine is no exception to this phenomenon. Clinical trials in several European countries then showed carbamazepine to be an effective antiepileptic drug. The reports that carbamazepine has a psychotropic effect and that it is effective in the treatment of manic-depressive illness is a reminder that its discovery was a byproduct of research on tricyclic antidepressants. Carbamazepine’s action resembles that of phenytoin in these experiments, in agreement with the similar effect of these two drugs against tonic-clonic seizures. It appears that carbamazepine and phenytoin bind to the neuron membrane to produce a use-, voltage-, and time-dependent block of sodium channels by slowing their recovery from inactivation.
