title: Novel model for the mechanisms of glutamate-dependent excitotoxicity: role of neuronal gap junctions.
abstract: 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.
authors: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA. abelousov@kumc.edu
authors: Andrei B
authors: AB
authors: Belousov
mesh_terms: D000818:Animals; D016923:Cell Death / Q000502:physiology; D002490:Central Nervous System / Q000254:growth & development / Q000293:injuries; D017630:Connexins / Q000378:metabolism; D017629:Gap Junctions / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D009474:Neurons / Q000502:physiology*
chemical_list: D017630:Connexins; D018698:Glutamic Acid