期刊
BRAIN RESEARCH
卷 1487, 期 -, 页码 123-130出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2012.05.063
关键词
Gap junction; Connexin 36; Neuronal death; Glutamate; Excitotoxicity
资金
- NIH [R01 NS064256, R21 NS076925]
- University of Kansas Medical Center
In the mammalian central nervous system (CNS), coupling of neurons by gap junctions (electrical synapses) increases during early post-natal development, then decreases, but increases in the mature CNS following neuronal injury, such as ischemia, traumatic brain injury and epilepsy. Glutamate-dependent neuronal death also occurs in the CNS during development and neuronal injury, i.e., at the time when neuronal gap junction coupling is increased. Here, we review our recent studies on the regulation of neuronal gap junction coupling by glutamate during development and injury and on the role of gap junctions in neuronal cell death. A novel model of the mechanisms of glutamate-dependent neuronal death is discussed, which includes neuronal gap junction coupling as a critical part of these mechanisms. (C) 2012 Elsevier B.V. All rights reserved.
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