Neuronal progenitor enrichment in the adult Cx32 knockout (KO) mouse.

Abstract

The connexin (Cx) family of channel-forming proteins is comprised of 15 or more members that form intercellular channels directly connecting the cytoplasm of adjacent cells (gap junctions). Cx proteins are found in both oligodendrocytes and neurons in the central nervous system (CNS) and myelinating Schwann cells in the peripheral nervous system (PNS). In humans, mutations in the gap junction Cx32 gene are associated with a inherited demyelinating disorder of the PNS, Charcot-Tooth-Marie disease (CMTX). In the CNS, Cx32 is one of the predominant Cxs expressed during the later stages of differentiation, neurogenesis, cell migration, and neural circuit formation. Thus, it is hypothesized that intracellular communication via Cx32-mediated channels plays a role in regional specification and arrangement of structures within the CNS. However, the impact of endogenous Cx32 expression and/or null mutation on neuronal differentiation have yet to be determined. To test the hypothesis that Cx32 expression influences CNS development, the cerebral development of Cx32 knockout (KO) mice was compared to that of wild-type (WT) littermate controls. (Abstract shortened by UMI.)