Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4353932 | Progress in Neurobiology | 2008 | 20 Pages |
Abstract
Brain hypoxia-ischemia is a relatively common and serious problem in neonates and in adults. Its consequences include long-term histological and behavioral changes and reduction in seizure threshold. Gap junction intercellular communication is pivotal in the spread of hypoxia-ischemia related injury and in mediating its long-term effects. This review provides a comprehensive and critical review of hypoxia-ischemia and hypoxia in the brain and the potential role of gap junctions in the spread of the neuronal injury induced by these insults. It also presents the effects of hypoxia-ischemia and of hypoxia on the state of gap junctions in vitro and in vivo. Understanding the mechanisms involved in gap junction-mediated neuronal injury due to hypoxia will lead to the development of novel therapeutic strategies.
Keywords
MCAOFVOalpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acidfreeze-fracture replica immunogold labelingN-methyl d-aspartateAGAconnexinsNBQXinositol triphosphateNMDARNMDAOGDIP3GFAPAMPAGJICcAMPAdenosine TriphosphateATPCyclic adenosine monophosphategap junctionsgap junctional intercellular communication18α-glycyrrhetinic acidmiddle cerebral artery occlusionfour-vessel occlusionepileptogenesisseizureTUNELCNScentral nervous systemFRILoxygen–glucose deprivationhypoxia–ischemiaglial acidic fibrillary proteinconnexinN-methyl d-aspartate receptor
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Authors
Rabih S. Talhouk, Michele P. Zeinieh, Mohamad A. Mikati, Marwan E. El-Sabban,