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Propofol post‐conditioning induced long‐term neuroprotection and reduced internalization of AMPAR GluR2 subunit in a rat model of focal cerebral ischemia/reperfusion
Author(s) -
Wang Haiyun,
Luo Mengqiang,
Li Cui,
Wang Guolin
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07400.x
Subject(s) - neuroprotection , propofol , ampa receptor , ischemia , glutamate receptor , internalization , reperfusion injury , anesthesia , medicine , hippocampus , neuroscience , neurogenesis , brain ischemia , pharmacology , receptor , psychology
J. Neurochem. (2011) 119 , 210–219. Abstract We previously reported that propofol (20 mg/kg/h) post‐conditioning provided acute (up to 24 h) neuroprotection in rats with transient middle cerebral artery occlusion. In this study, we extend these data by examining long‐term protection and exploring underlying mechanisms involving AMPA receptor GluR2 subunit internalization. Rats were treated with propofol 20 mg/kg/h after 60 min of occlusion (beginning of reperfusion for 4 h). Propofol post‐conditioning reduced infarct volume and improved spatial memory deficiencies (up to 28 days) induced by ischemia/reperfusion injury. Additionally, Propofol post‐conditioning promoted neurogenesis in the dentate gyrus of hippocampus, as measured by bromodeoxyuridine and neuron‐specific nuclear protein immunofluorescence‐double staining at day 28 after reperfusion. Finally, propofol post‐conditioning increased the surface expression of AMPA receptor GluR2 subunit, thus inhibited the internalization of this part until 28 days after stroke. In conclusion, our data suggest that propofol post‐conditioning provides long‐term protection against focal cerebral ischemia/reperfusion injury in rats. Furthermore, we found that the inhibition of AMPA receptor GluR2 subunit internalization may contributed to this long‐term neuroprotection.