Hood T W, Siegfried J, Haas H L
Cell Mol Neurobiol. 1983 Sep;3(3):213-22. doi: 10.1007/BF00710948.
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.
在低钙、高镁溶液中,治疗浓度的卡马西平对大鼠海马切片CA1区的自发放电场爆发有强烈抑制作用。卡马西平降低大鼠海马切片的兴奋性和突触传递,且对强直后增强无影响,这与先前关于脊髓和外周神经的研究一致。卡马西平对突触抑制和超极化后电位无影响,而戊巴比妥和腺苷分别显著增强了这些抑制过程。自发放电场爆发至少部分是通过电场耦合传播同步的,可作为癫痫和三叉神经痛的模型。卡马西平在这两种疾病中的临床疗效可能是通过抑制这种病理性同步来解释的。