Abstract
Electroconvulsive shock (ECS) has long been used for treatment of psychiatric diseases including manic-depressive illness. Its clinical benefits have been repeatedly documented in medically resistant cases or particularly serious cases that would otherwise end up with suicide. How ECS works is not known. We have developed a rat model for studying mechanisms by which ECS is made effective. Electrophysiological recordings and calcium photometry were done in visual cortex slices obtained from ECS-subjected rats. Two remarkable findings have come out in our recent experiments. First, resting membrane potential was unusually hyperpolarized, and spike firing in response to depolarizing currents were decreased. Second, L-type voltage-dependent calcium channels were upregulated, with action potential-induced calcium influx enhanced, thereby facilitating calcium spike generation. The ECS-induced hyperpolarization is reminiscent of the effects of the minor tranquilizer benzodiazepin, which facilitates GABA-A receptors and favors hyperpolarization. The combined occurrence of calcium spike facilitation and spike firing attenuation may have a serious impact on synaptic efficiency in the framework of theoretical models of Hebbian plasticity and spike timing-dependent plasticity. According to these models, the two effects combined together are suggested to bias synaptic plasticity in favor of synaptic downregulation or downscaling. Such downscaling of synaptic efficiency might contribute to disruption of abnormal neural states. [Jpn J Physiol 55 Suppl:S56 (2005)]
