Impact Of Astrocytic Gap Junction On The Hypoperfusion Induced Deep White Matter Injury

Purpose:To study the changes about the expression of myelin associated protein MAG and MBP in mice after conducting BCAS different times and the influence on the white matter injury induced by hypoperfusion brought by knocking out the protein connexin43 of astrocytes.To observe the difference of oligodendrocytes proliferation.Methods: The Cre- lox P technology is used to get the C57 mice with knockout connexin43 of astrocytes C57 mice, bilateral common carotid artery stenosis technology is used to establish the brain white matter hypoperfusion model. Through the protein immunoblot method, myelin associated protein of the different experimental groups could be semi-quantitated. Using immunofluorescence staining techniques to observe the proliferation and differentiation of oligodendrocytes in experimental mice white matter and the changes about the structure of the node of ranvier.Results: In BCAS model, the condition of hypoperfusion can lead to a potential white matter demyelination changes and the decrease of mature oligodendrocytes. However,K nocking out cx43 of astrocytes can reduce the extent of the demyelination, the apoptosis of mature oligodendrocytes and lighten the changes in the structure of axons node of ranvier.Conclusions: That knocking out astrocytes cx43 can relieve cerebral white matter lesions caused by hypoperfusion and has certain nerve protective effect.Objective: Study the effects of specific regulation of astrocyte C x43 on hypoperfusion induced damage of cerebral white matter, exploring the mechanism of gap junction channels mediated communication in the hypoperfusion induced white matter injury.Methods:The technology of microdialysis could be used to dialysis small molecules in the white matter of different experimental groups.Fluorescent of chemical and electrochemical methods could be used to detect the concentration of different types of small molecules in dialysate,such as lactic acid, glutamate and adenosine. The technology of 1H-NMR is used to detect the change of metabolite in the area of whiter matter.Results: Under physiological conditions, the knockout of specific protein gap junction Cx43 of astrocytes in mice brain did not affect the micro-environment of white matter significantly.When mice are suffered hypoperfusion induced cerebral white matter damage for 3 days,the concentration of adenosine, lactic acid and glutamic acid increased obviously.While,that in mice with knockout of C x43 increased mildly.Conclusions:That knocking out gap junction Cx43 in astrocytes has no obvious influence on mice under normal condition, but it could protect mouse from injury and keep the micro-environment of white matter stability under long hypoperfusion.