期刊
PHARMACOLOGY & THERAPEUTICS
卷 87, 期 2-3, 页码 151-159出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0163-7258(00)00045-0
关键词
adenosine; N-6-(R)-phenylisopropyladenosine (R-PIA); 1,2-dioctanoyl-rac-glycerol (DOG); protein kinase C (PKC); ATP-sensitive potassium (K-ATP) channels; glibenclamide
Neurons can be preconditioned by various procedures to resist ischemic insult. The preconditioning mechanism induced by adenosine (the adenosine mechanism) was characterized in primary rat neuronal cultures, employing a model of chemical ischemia. The protective mechanism, initiated by activation of adenosine receptors, consists of a signal transduction pathway, involving activation of protein kinase C (PKC) and opening of ATP-sensitive potassium (K-ATP) channels. Direct activation (and inhibition) of PKC, as well as opening of K-ATP channels, also confers protection. The opening of the K-ATP channels mediates the signal activated by the adenosine receptors, and probably also that activated by PKC. The acquired ischemic resistance lasts up to 5 days, depending on the activating substance. The adenosine-activated cascade of events leading to ischemic tolerance in neurons is similar to that operating in cardiomyocytes. (C) 2000 Elsevier Science Inc. All rights reserved.
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