TY - JOUR
T1 - Ischemic tolerance conferred to cultured rat neurons by heat shock is not mediated by opening of adenosine triphosphate-sensitive potassium channels
AU - Reshef, Ayelet
AU - Capua, Noam Di
AU - Sperling, Oded
AU - Zoref-Shani, Esther
N1 - Funding Information:
This work partially fulfills the requirements of the PhD thesis of A.R. and N.D. at the Sackler Faculty of Medicine, Tel Aviv University. The study was supported by grants from the Heller Fund for Medical Research of the Sackler Faculty of Medicine and from the Adams Super-Center for Brain Studies of Tel-Aviv University.
PY - 2000/6/30
Y1 - 2000/6/30
N2 - The effect of sublethal heat shock on the capacity of neurons to resist subsequent ischemia-reperfusion-induced cell injury, was studied in a model of primary rat neuronal cultures, subjected to chemical ischemia. Exposure of the cultures to sublethal heat shock (42°C; 20 min) resulted in elevation in cellular content of heat shock protein (HSP)-70, at 4 h following the shock, and in acquisition of a 15 h 'time window of protection' against ischemia-reperfusion insult, with maximum protection at 4 h. Presence in the culture medium of glibenclamide (2 μM), a blocker of ATP sensitive potassium (K(ATP)) channels, did not abolish the acquisition of protection throughout the entire duration of the acquired 'time window of protection'. The results demonstrate that heat shock induces in neurons a protective mechanism against ischemia-reperfusion insult, probably associated with enhanced expression of HSPs, which does not depend on opening of K(ATP) channels. In this respect, the neuronal 'heat-shock mechanism' for the acquisition of ischemic tolerance differs from the neuronal 'adenosine mechanism' and probably also from the heart 'heat shock mechanism' for the acquisition of protection. Copyright (C) 2000 Elsevier Science Ireland Ltd.
AB - The effect of sublethal heat shock on the capacity of neurons to resist subsequent ischemia-reperfusion-induced cell injury, was studied in a model of primary rat neuronal cultures, subjected to chemical ischemia. Exposure of the cultures to sublethal heat shock (42°C; 20 min) resulted in elevation in cellular content of heat shock protein (HSP)-70, at 4 h following the shock, and in acquisition of a 15 h 'time window of protection' against ischemia-reperfusion insult, with maximum protection at 4 h. Presence in the culture medium of glibenclamide (2 μM), a blocker of ATP sensitive potassium (K(ATP)) channels, did not abolish the acquisition of protection throughout the entire duration of the acquired 'time window of protection'. The results demonstrate that heat shock induces in neurons a protective mechanism against ischemia-reperfusion insult, probably associated with enhanced expression of HSPs, which does not depend on opening of K(ATP) channels. In this respect, the neuronal 'heat-shock mechanism' for the acquisition of ischemic tolerance differs from the neuronal 'adenosine mechanism' and probably also from the heart 'heat shock mechanism' for the acquisition of protection. Copyright (C) 2000 Elsevier Science Ireland Ltd.
KW - Adenosine
KW - Adenosine triphosphate-sensitive potassium channels
KW - Glibenclamide
KW - Heat shock
KW - Heat shock protein
KW - Ischemia-reperfusion damage
KW - Ischemic tolerance
KW - Neuronal cultures
UR - http://www.scopus.com/inward/record.url?scp=0034733830&partnerID=8YFLogxK
U2 - 10.1016/S0304-3940(00)01190-3
DO - 10.1016/S0304-3940(00)01190-3
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AN - SCOPUS:0034733830
SN - 0304-3940
VL - 287
SP - 223
EP - 226
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -