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Trends Neurosci. 2013 Apr;36(4):227-36. doi: 10.1016/j.tins.2012.11.001. Epub 2012 Dec 11.

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

Author information

1
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA. abelousov@kumc.edu

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.

PMID:
23237660
PMCID:
PMC3609876
DOI:
10.1016/j.tins.2012.11.001
[Indexed for MEDLINE]
Free PMC Article

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