Neuronal gap junctions: making and breaking connections during development and injury

• Published in: Trends in neurosciences (Regular ed.) Vol. 36; no. 4; pp. 227 - 236
• Main Authors: Belousov, Andrei B, Fontes, Joseph D
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-04-2013; Elsevier Sequoia S.A
• Subjects: Animals; Brain damage; Brain Diseases - pathology; brain trauma; Central Nervous System - cytology; Central Nervous System - growth & development; Central Nervous System - injuries; connexin 36; Connexins - metabolism; development; Electrical Synapses - physiology; Gap Junction delta-2 Protein; gap junctions; Gene expression; glutamate excitotoxicity; Humans; Mammals; Monoclonal antibodies; Nervous system; Neurology; Neurosciences; stroke; connexin 36; gap junctions; glutamate excitotoxicity; development; stroke; brain trauma
• ISSN: 0166-2236; 1878-108X
• DOI: 10.1016/j.tins.2012.11.001

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.