The gap junctions (GJs), which form intercellular communicating channels between two apposing cells or formhemichannel with extracellular environment, perform crucial functions to maintain small molecule homeostasis. Thecentral nervous system (CNS) GJs are important for maintenance of myelin sheath and neuronal activity. Connexin (Cx)proteins are building blocks of GJs. Recent cell-biological investigations show that amongst the CNS specific Cxs, themost abundant Cx protein, Cx43 and its oligodendrocytic coupling partner Cx47 primarily important for maintenance ofCNS myelin. Recent investigations elucidate that the expression of Cx43 and Cx47 is very important to maintain K?buffering and nutrient homeostasis in oligodendrocytes, CNS myelin and oligodendrocyte function. The investigationson Multiple Sclerosis (MS) patient samples and EAE hypothesized that the functional loss of Cx43/Cx47 could beassociated with spread of chronic MS lesions. Exploring the mechanism of initial GJ alteration and its effect ondemyelination in this model of MS might play a primary role to understand the basis of altered CNS homeostasis,observed during MS. In this review, we mainly discuss the role of CNS GJs, specifically the Cx43/Cx47 axis in theperspective of demyelination.
Volume 44 | Issue 6
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