TY - JOUR
T1 - The adenosine-induced mechanism for the acquisition of ischemic tolerance in primary rat neuronal cultures
AU - Reshef, Ayelet
AU - Sperling, Oded
AU - Zoref-Shani, Esther
N1 - Funding Information:
The results of A.R. included in this review are in partial fulfillment of the requirements for the Ph.D. degree at the Sackler Faculty of Medicine, Tel Aviv University. These studies were supported in part by the Basic Research Fund and by the Adams Super-center for Brain Studies of Tel-Aviv University.
PY - 2000/8
Y1 - 2000/8
N2 - 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.
AB - 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.
KW - 1,2-dioctanoyl-rac- glycerol (DOG)
KW - ATP-sensitive potassium (K(ATP)) channels
KW - Adenosine
KW - Glibenclamide
KW - N-(R)-phenylisopropyladenosine (R-PIA)
KW - Protein kinase C (PKC)
UR - http://www.scopus.com/inward/record.url?scp=0033796893&partnerID=8YFLogxK
U2 - 10.1016/S0163-7258(00)00045-0
DO - 10.1016/S0163-7258(00)00045-0
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
AN - SCOPUS:0033796893
SN - 0163-7258
VL - 87
SP - 151
EP - 159
JO - Pharmacology and Therapeutics
JF - Pharmacology and Therapeutics
IS - 2-3
ER -