title: Neuronal gap junction coupling as the primary determinant of the extent of glutamate-mediated excitotoxicity.
abstract: 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.
authors.affiliation: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 2146 W. 39th Avenue, M/S 3051, Kansas City, KS, 66160, USA, abelousov@kumc.edu.
authors.forename: Andrei B
authors.initials: AB
authors.lastname: Belousov
authors.forename: Joseph D
authors.initials: JD
authors.lastname: Fontes
mesh_terms: D000818:Animals; D016923:Cell Death / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D002490:Central Nervous System / Q000254:growth & development / Q000502:physiology / Q000503:physiopathology; D017629:Gap Junctions / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism*; D006801:Humans; D009474:Neurons / Q000502:physiology*
chemical_list: D018698:Glutamic Acid