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TRPC6 expression in neurons is differentially regulated by NR2A- and NR2B-containing NMDA receptors.

Authors
  • Qu, Zhongwei1, 2
  • Wang, Yuqing1, 2
  • Li, Xia3
  • Wu, Lin3
  • Wang, Yizheng1, 3
  • 1 Laboratory of Neural Signal Transduction, Institute of Neuroscience, Chinese Academy of Sciences, Shanghai, China. , (China)
  • 2 The Graduate School, University of Chinese Academy of Sciences, Beijing, China. , (China)
  • 3 Center of Cognition and Brain Science, Beijing Institute of Medical Sciences, Beijing, China. , (China)
Type
Published Article
Journal
Journal of Neurochemistry
Publisher
Wiley (Blackwell Publishing)
Publication Date
Nov 01, 2017
Volume
143
Issue
3
Pages
282–293
Identifiers
DOI: 10.1111/jnc.14215
PMID: 28902407
Source
Medline
Keywords
License
Unknown

Abstract

The expression of transient receptor potential canonical 6 (TRPC6) in central nervous system (CNS) is important for neuronal functions and certain neural disorders. However, the regulatory mechanism of TRPC6 expression in neurons is still obscure. In this study, we show that TRPC6 expression in the primary cultured cortical neurons is bidirectionally regulated by glutamate. Activation of NR2A-containing NMDARs induces TRPC6 transcription through a calcineurin-dependent pathway. In contrast, activation of NR2B-containing NMDARs causes TRPC6 degradation through calpain. Thus, TRPC6 expression in neurons is regulated by glutamate in a bidirectional manner that is dependent on NR2A and NR2B.

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