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Neuronal gap junctions: making and breaking connections during development and injury
Andrei B Belousov1, Joseph D Fontes
1Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA. abelousov@kumc.edu
Trends in Neurosciences
|December 15, 2012
Summary
Neuronal gap junctions, including connexin 36 (Cx36), increase during development and after CNS injury. These electrical synapses play roles in neuronal function and glutamate-mediated cell death.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- Neuronal gap junctions, mediated by connexin 36 (Cx36), are crucial for CNS development.
- Cx36 expression and neuronal coupling are transiently high in early development, declining in adulthood.
Purpose of the Study:
- To summarize new findings on Cx36 regulation in the CNS.
- To review the roles of neuronal gap junctions, especially in injury and excitotoxicity.
Main Methods:
- Review of recent studies on Cx36 regulation.
- Analysis of literature on neuronal gap junction function.
Main Results:
- Cx36 expression and coupling increase during early development and following CNS injury (ischemia, TBI, epilepsy).
- Cx36 levels are low in adult neurons but present in specific subsets.
- Neuronal gap junctions have diverse roles, including involvement in glutamate-mediated neuronal death.
Conclusions:
- Cx36 expression and gap junction coupling are dynamically regulated in the CNS.
- Neuronal gap junctions are implicated in pathological processes like excitotoxicity.
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