学术报告

题目：CaV3.2 calcium channels control NMDA transmission at synapses

报告人：Dr. Guangfu Wang

时间：2016年2月19日（周五）13:00-14:00

地点：英国威廉希尔公司王克桢楼348室

摘要：

CaV3.2 T-type calcium channels, encoded by CACNA1H, are expressed throughout the brain, yet their general function remains unclear. We discovered that CaV3.2 channels control NMDA-sensitive glutamatergic receptor (NMDA-R)-mediated transmission and subsequent NMDA-R-dependent plasticity of AMPA-R-mediated transmission at rat central synapses. Interestingly, functional CaV3.2 channels primarily incorporate into synapses, replace existing CaV3.2 channels, and can induce local calcium influx to control NMDA transmission strength in an activity dependent manner. Moreover, human childhood absence epilepsy (CAE)-linked hCaV3.2(C456S) mutant channels have a higher channel open probability, induce more calcium influx, and enhance glutamatergic transmission. Remarkably, cortical expression of hCaV3.2(C456S) channels in rats induces 2- to 4-Hz spike and wave discharges and absence-like epilepsy characteristic of CAE patients, which can be suppressed by AMPA-R and NMDA-R antagonists but not T-type calcium channel antagonists. These results reveal an unexpected role of CaV3.2 channels in regulating NMDA-R-mediated transmission and a novel epileptogenic mechanism for human CAE.

报告人简介:

With a solid background of physics and more than 7 years of experience in neuroscience, I developed a series of cutting-edge techniques, and employed them to study neuronal circuits and synaptic plasticity. Most importantly, I successfully collaborated with other researchers (both inside and outside UVa), and generated several peer-reviewed publications for each project. The prior experience prepared me with the necessary expertise, leadership and motivation, as well as the necessary technology, to be successfully competent for future academic research.

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