Belousov Andrei B, Fontes Joseph D
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 2146 W. 39th Avenue, M/S 3051, Kansas City, KS, 66160, USA,
J Neural Transm (Vienna). 2014 Aug;121(8):837-46. doi: 10.1007/s00702-013-1109-7. Epub 2013 Nov 1.
In the mammalian central nervous system (CNS), coupling of neurons by gap junctions (electrical synapses) increases during early postnatal 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 regulation of neuronal gap junction coupling by glutamate in developing and injured neurons and on the role of gap junctions in neuronal cell death. A modified model of the mechanisms of glutamate-dependent neuronal death is discussed, which includes neuronal gap junction coupling as a critical part of these mechanisms.
在哺乳动物的中枢神经系统（CNS）中，间隙连接（电突触）介导的神经元耦合在出生后早期发育过程中增加，随后减少，但在成熟的中枢神经系统中，在诸如缺血、创伤性脑损伤和癫痫等神经元损伤后会再次增加。在发育过程和神经元损伤期间，即神经元间隙连接耦合增加时，中枢神经系统中也会发生谷氨酸依赖性神经元死亡。在这里，我们回顾了我们最近关于发育中和受损神经元中谷氨酸对神经元间隙连接耦合的调节以及间隙连接在神经元细胞死亡中的作用的研究。我们还讨论了谷氨酸依赖性神经元死亡机制的修正模型，其中包括神经元间隙连接耦合作为这些机制的关键部分。
