title: Neuronal gap junctions: making and breaking connections during development and injury.
abstract: In the mammalian central nervous system (CNS), coupling of neurons by gap junctions (i.e., electrical synapses) and the expression of the neuronal gap junction protein, connexin 36 (Cx36), transiently increase during early postnatal development. The levels of both subsequently decline and remain low in the adult, confined to specific subsets of neurons. However, following neuronal injury [such as ischemia, traumatic brain injury (TBI), and epilepsy], the coupling and expression of Cx36 rise. Here we summarize new findings on the mechanisms of regulation of Cx36-containing gap junctions in the developing and mature CNS and following injury. We also review recent studies suggesting various roles for neuronal gap junctions and in particular their role in glutamate-mediated neuronal death.
authors.affiliation: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 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; D001927:Brain Diseases / Q000473:pathology*; D002490:Central Nervous System / Q000166:cytology / Q000254:growth & development / Q000293:injuries; D017630:Connexins / Q000378:metabolism*; D054351:Electrical Synapses / Q000502:physiology*; D006801:Humans; D000097004:Gap Junction delta-2 Protein
chemical_list: D017630:Connexins; D000097004:Gap Junction delta-2 Protein