Effect of hippocampal electrical stimulation on the sodium channel current in CA1 region neurons in rats with pharmacoresistant temporal lobe epilepsy
10.3760/cma.j.issn.1006-7876.2013.08.003
- VernacularTitle:海马电刺激对耐药性颞叶癫痫大鼠CA1区神经元钠通道电流的影响
- Author:
Guofeng WU
;
Zhen HONG
;
Binli GAO
;
Feng ZHOU
- Publication Type:Journal Article
- Keywords:
Epilepsy,temporal lobe;
Hippocampus;
Electric stimulation;
Sodium channels;
Drug resistance,multiple;
Kindling,neurologic;
Disease models,animal
- From:
Chinese Journal of Neurology
2013;46(8):513-518
- CountryChina
- Language:Chinese
-
Abstract:
Objective To establish a multi-drug resistant model of temporal lobe epilepsy,and then the sodium current of pyramidal neurons in CA1 areas of the hippocampus was used as as index to observe the effect of hippocampal stimulation on pharmacoresistant epileptic rats.Methods Eighty Wistar rats were selected to prepare an amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.When the kindled model of epilepsy was prepared successfully,the pharmacoresistant epileptic rats were selected according their response to phenobabital and phenytoin.The selected pharmacoresistant epileptic rats were divided into a hippocampal stimulation group (HS group) and a pharmacoresistant control group (PR group).A low-frequency hippocampal stimulation was performed in the HS group,while the PR group received sham stimulation.The whole-cell recording technique by patch-clamp was used to observe the changes of sodium current of hippocampal pyramidal neurons after the hippocampal stimulation.Results Compared with the PR group,the pharmacoresistant epileptic rats in HS group underwent low-frequency stimulation for 2 weeks showed that the amygdale stimulus-induced seizures were decreased (2.32 ± 0.38 in HS group and 4.45 ± 0.42 in PR group,t =84.600,P =0.000) and the parameters of the after-discharges were improved significantly.In HS group,the peak current shifted towards depolarization,the sodium channels were difficult to activate,and were more susceptible to inactivation.Moreover,the recovery time after the sodium channel inactivation was slower in HS group ((17.9 ±0.6) s) than in PR group((16.3 +0.3) s,t =-25.420,P =0.000).Conclusions Hippocampal stimulation may inhibit the sodium channel current of pyramidal neurons in CA1 areas of hippocampus.The mechanism of hippocampal stimulation in the treatment of pharmacoresistant epilepsy might be achieved partly by inhibiting the sodium channel current so as to decrease the excitability of hippocampal neurons.
