作者: Emanuela Viggiano , Davide Viggiano , Alessandro Viggiano , Bruno De Luca , Marcellino Monda
DOI: 10.1007/S11064-014-1447-3
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摘要: Cortical spreading depression (CSD) enhances ischemic tolerance to temporary focal ischemia. Although this effect most likely requires the expression or activation of neuroprotective factors, their identity remains relatively unknown. One important factor involved in neuroprotection is adenosine monophosphate-dependent kinase (AMPK), a serine/threonine that activated via phosphorylation. This occurs response brain ischemia, hypoxia, glucose deprivation. Thus, determine potential mechanism effects CSD, we tested whether AMPK becomes phosphorylated into phospho-AMP-activated protein (pAMPK) after CSD. CSD was induced for 15 min three groups five rats. The animals were subsequently sacrificed 2, 4 24 h. Western blot analyses performed AMPKα and pAMPKα levels cortex (right left hemispheres), immunohistochemistry immunofluorescence localisation cerebral cortex. These results demonstrated significant increase at 24 h (but not 2 4 h) In contrast, un-phosphorylated did change. confined neurons (predominantly located superficial layers cortex) observed astroglial cells. Taken together, these data indicate by suggest may contribute