CaV3.2 calcium channels control NMDA receptor-mediated transmission: a new mechanism for absence epilepsy.

@article{Wang2015CaV32CC,
  title={CaV3.2 calcium channels control NMDA receptor-mediated transmission: a new mechanism for absence epilepsy.},
  author={Guangfu Wang and Genrieta Bochorishvili and Yucai Chen and Kathryn A Salvati and Peng Zhang and Steve J Dubel and Edward Perez-Reyes and Terrance P. Snutch and Ruth L Stornetta and Karl Deisseroth and Alev Erisir and Slobodan M Todorovic and Jianhong Luo and Jaideep Kapur and Mark P. Beenhakker and Jinsong Zhu},
  journal={Genes & development},
  year={2015},
  volume={29 14},
  pages={1535-51}
}
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… CONTINUE READING
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