• I-Hui Lee, Eva Lindqvist, Ole Kiehn, Johan Widenfalk, and Lars Olson.
• Department of Neuroscience, Karolinska Institute, 17177 Stockholm, Sweden. i-hui.lee@neuro.ki.se
• J. Comp. Neurol. 2005 Aug 15; 489 (1): 1-10.

AbstractSpinal cord injury induces a complex cascade of degenerative and remodeling events evolving over time. The possible roles of changed intercellular communication via gap junctions after spinal cord injury (SCI) have remained relatively unexplored. We investigated the temporospatial expression patterns of gap junctional genes and proteins, connexin 43 (Cx43), Cx36, and Cx32, by in situ hybridization and immunohistochemistry in the rat neonatal, adult normal, and adult injured spinal cord. Cx36 was strongly expressed in immature neurons, and levels declined markedly during development, whereas Cx43 and Cx32 persisted throughout adulthood. After a complete transection of the adult spinal cord, the levels of Cx43 mRNA and protein were up-regulated within hours, especially in gray matter rostral to the lesion, reaching over three times normal levels at 4 weeks postinjury. Cx43 immunoreactivity was seen primarily in astrocytes and rarely in microglia. In contrast, Cx36 and Cx32 mRNA and proteins were relatively sparse and unchanged after spinal cord injury along the entire axis of the spinal cord. Cx43 is the most abundant gap junctional protein in the adult CNS and has been shown to form channels between astrocytes as well as between astrocytes and oligodendrocytes. Long-term up-regulation of Cx43 in reactive astrocytes may be one critical component in the rearrangement of the local astroglial network following SCI.Copyright (c) 2005 Wiley-Liss, Inc.

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