期刊
NEUROSCIENCE LETTERS
卷 524, 期 1, 页码 16-19出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2012.06.065
关键词
Gap junctions; Connexin 36; Traumatic brain injury; Glutamate; Neuronal death
资金
- NIH [R01 NS064256, R21 NS076925]
- University of Kansas Medical Center funds
In the mammalian CNS, excessive release of glutamate and overactivation of glutamate receptors are responsible for the secondary (delayed) neuronal death following neuronal injury, including ischemia, traumatic brain injury (TBI) and epilepsy. Recent studies in mice showed a critical role for neuronal gap junctions in NMDA receptor-mediated excitotoxicity and ischemia-mediated neuronal death. Here, using controlled cortical impact (CCI) in adult mice, as a model of TBI, and Fluoro-jade B staining for analysis of neuronal death, we set to determine whether neuronal gap junctions play a role in the CCI-mediated secondary neuronal death. We report that 24 h post-CCI, substantial neuronal death is detected in a number of brain regions outside the injury core, including the striatum. The striatal neuronal death is reduced both in wild-type mice by systemic administration of mefloquine (a relatively selective blocker of neuronal gap junctions) and in knockout mice lacking connexin 36 (neuronal gap junction protein). It is also reduced by inactivation of group II metabotropic glutamate receptors (with LY341495) which, as reported previously, control the rapid increase in neuronal gap junction coupling following different types of neuronal injury. The results suggest that neuronal gap junctions play a critical role in the CO-induced secondary neuronal death. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
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