کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4324957 | 1613952 | 2012 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Novel model for the mechanisms of glutamate-dependent excitotoxicity: Role of neuronal gap junctions Novel model for the mechanisms of glutamate-dependent excitotoxicity: Role of neuronal gap junctions](/preview/png/4324957.png)
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.
Journal: Brain Research - Volume 1487, 3 December 2012, Pages 123–130