Abstract
Carbamazepine at therapeutic concentrations has a strong inhibitory effect on the spontaneous field bursts of the CA 1 region of rat hippocampal slices in low-Ca2+, high-Mg2+ solution. A reduction of excitability and synaptic transmission as well as no effect on posttetanic potentiation in the rat hippocampal slice by carbamazepine agrees with previous studies on spinal cord and peripheral nerve. Carbamazepine left synaptic inhibition and hyperpolarizing afterpotentials unaltered while these inhibitory processes were markedly enhanced by pentobarbital and adenosine, respectively. The spontaneous field bursts are, at least in part, synchronized by ephaptic transmission and may serve as a model of epilepsy and trigeminal neuralgia. The clinical effectiveness of carbamazepine in these two ailments may be explained by a suppression of this pathological synchronization.