Depression of neuronal excitability and epileptic activities by group II metabotropic glutamate receptors in the medial entorhinal cortex.
Depression of neuronal excitability and epileptic activities by group II metabotropic glutamate receptors in the medial entorhinal cortex.
复制标题
内侧内嗅皮层 II 类代谢型谷氨酸受体抑制神经元兴奋性和癫痫活动。
DOI：
10.1002/hipo.22437
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发表时间：
2015
期刊：
影响因子：
3.5
通讯作者：
Lei,Saobo
中科院分区：
文献类型：
--
作者：
Zhang,Haopeng;Cilz,NicholasI;Yang,Chuanxiu;Hu,Binqi;Dong,Hailong;Lei,Saobo
Whereas the ionotropic glutamate receptors are the major mediator in glutamatergic transmission, the metabotropic glutamate receptors (mGluRs) usually play a modulatory role. Whereas the entorhinal cortex (EC) is an essential structure involved in the generation and propagation of epilepsy, the roles and mechanisms of mGluRs in epilepsy in the EC have not been determined. Here, we studied the effects of activation of group II metabotropic glutamate receptors (mGluRs II) on epileptiform activity induced by picrotoxin or deprivation of extracellular Mg2+and neuronal excitability in the medial EC. We found that activation of mGluRs II by application of the selective agonist, LY354740, exerted robust inhibition on epileptiform activity. LY354740 hyperpolarized entorhinal neurons via activation of a K+conductance and inhibition of a Na+‐permeable channel. LY354740‐induced hyperpolarization was G protein‐dependent, but independent of adenylyl cyclase and protein kinase A. However, the function of Gβγ was involved in mGluRs II‐mediated depression of both neuronal excitability and epileptiform activity. Our results provide a novel cellular mechanism to explain the antiepileptic effects of mGluRs II in the treatment of epilepsy. © 2015 Wiley Periodicals, Inc.
