Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 51, Pages 13949-13957Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3395-07.2007
Keywords
gap junction; glia; myelin; connexin; astrocytes; oligodendrocytes
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Funding
- NINDS NIH HHS [NS050705, NS054363, K02 NS050345-03, R01 NS050705-03, NS043560, NS50345, K02 NS050345-02, NS55284, R01 NS050705-02, R01 NS050705, K02 NS050345] Funding Source: Medline
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Genetic diseases demonstrate that the normal function of CNS myelin depends on connexin 32 (Cx32) and Cx47, gap junction (GJ) proteins expressed by oligodendrocytes. GJs couple oligodendrocytes and astrocytes (O/A channels) as well as astrocytes themselves (A/A channels). Because astrocytes express different connexins (Cx30 and Cx43), O/A channels must be heterotypic, whereas A/A channels may be homotypic or heterotypic. Using electrophysiological and immunocytochemical approaches, we found that Cx47/Cx43 and Cx32/Cx30 efficiently formed functional channels, but other potential heterotypic O/A and A/A pairs did not. These results suggest that Cx30/Cx30 and Cx43/Cx43 channels mediate A/A coupling, and Cx47/Cx43 and Cx32/Cx30 channels mediate O/A coupling. Furthermore, Cx47/Cx43 and Cx32/Cx30 channels have distinct macroscopic and single-channel properties and different dye permeabilities. Finally, Cx47 mutants that cause Pelizaeus-Merzbacher-like disease do not efficiently form functional channels with Cx43, indicating that disrupted Cx47/Cx43 channels cause this disease.
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