Glial Communication via Gap Junction in Neuroinflammation
Gap junction is the major intercellular channel that facilitates direct signaling between cytoplasmic compartments of adjacent cells by transferring various small molecules (~1,000 Da) and ions. Gap junction consists of a pair of hemichannels, each of which is a hexameric cluster of protein subunits named connexin. Recent studies have revealed that uncoupled “free” hemichannels also facilitate two-way transfer of molecules between the cytosol and extracellular space. In the central nervous system (CNS), gap junctions and hemichannels form the neuron–glia network and contribute to the maintenance of homeostasis by propagating signals and buffering against toxins. Other evidence suggests that gap junctions and hemichannels—especially in glial cells—are also involved in the initiation and amplification of neuroinflammation in various neurological disorders. The purpose of this review is to summarize recent insights into the roles of gap junctions and hemichannels in the physiologic and pathologic conditions of the CNS.
KeywordsAmyotrophic Lateral Sclerosis Experimental Autoimmune Encephalomyelitis Glycyrrhetinic Acid Connexin Gene Connexin Channel
This work was supported by the Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation (NIBIO); grants from the Ministry of Health, Labour and Welfare of Japan; a grant-in-aid for Scientific Research on Innovative Areas; and a grant-in-aid for the Global Center of Excellence Program from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
Conflicts of interest The author has no conflicts of interest to declare.
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