Literature DB >> 17640036

Expression of connexins in embryonic mouse neocortical development.

Cima Cina1, John F Bechberger, Mark A Ozog, Christian C G Naus.   

Abstract

During embryonic development, young neurons migrate from the ventricular zone to the cortical plate of the cerebral cortex. Disturbances in this neuronal migration have been associated with numerous diseases such as mental retardation, double cortex, Down syndrome, and epilepsy. One possible cause of these neuropathologies is an aberration in normal gap junctional communication. At least 20 connexin (Cx) genes encode gap junction proteins in mice and humans. A proper understanding of the role of specific connexins in the developing brain requires the characterization of their spatial and temporal pattern of expression. In the current study we performed all the experiments on mouse developing cortex at embryonic days (E) 14, 16, and 18, timepoints that are highly active with regard to cortical development. Using reverse transcription-polymerase chain reaction, Western blot analysis, and immunohistochemistry, we found that among the family of gap junction proteins, Cx26, Cx36, Cx37, Cx43, and Cx45 were expressed in the developing cortex of mice, Cx30 and Cx32 were absent, while Cx40 was expressed at a very low level. Our results demonstrate that Cx26 and Cx37 were evenly distributed in the cortical layers of developing brain, while Cx36 and Cx43 were more abundant in the ventricular zone and cortical plate. Cx45 distribution appeared to be more abundant at E18 compared to the other timepoints (E14 and E16). Thus, the present study provides identification and the distribution pattern for Cxs associated with cortical development during normal neuronal migration. Copyright (c) 2007 Wiley-Liss, Inc.

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Year:  2007        PMID: 17640036     DOI: 10.1002/cne.21426

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


  42 in total

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Review 5.  Neuronal gap junction coupling as the primary determinant of the extent of glutamate-mediated excitotoxicity.

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Review 8.  The role of connexins during early embryonic development: pluripotent stem cells, gene editing, and artificial embryonic tissues as tools to close the knowledge gap.

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Review 9.  Modulation of brain hemichannels and gap junction channels by pro-inflammatory agents and their possible role in neurodegeneration.

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