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Ischemic postconditioning protects against cerebral ischemia/reperfusion‐induced calcium overload in mice
Author(s) -
SHEN Jia,
ZHOU Jingyi,
PENG Yunlong,
XIA Qiang
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.614.18
Subject(s) - nmda receptor , ischemia , calcium , antagonist , anesthesia , medicine , dizocilpine , excitotoxicity , pharmacology , glutamate receptor , hippocampus , reperfusion injury , calcium in biology , chemistry , receptor
OBJECTIVE This study was to investigate whether postconditioning could reduce ischemia/reperfusion (I/R) induced calcium overload in neurons and the relative mechanism. METHODS Male C57BL/6 mice (23‐28g) were randomly divided into Sham (PBS injection without ischemia) group, Control (PBS injection with ischemia/reperfusion) group, Postconditioning (PBS injection, ischemia followed by 3 circles of 15 sec reperfusion and 15 sec occlusion before permanent reperfusion) group (PC group), N‐methyl‐D‐aspartate (NMDA receptor activator, NMDA) injection + PC group (NMDA group), MK‐801 (NMDA receptor non‐competitive antagonist) injection + PC group (MK‐801 group). Intracerebroventricular injections of PBS, NMDA or MK‐801 respectively were performed 30 min before 15min period of global ischemia. Two hours after reperfusion, acute hippocampus slices were prepared for intracellular calcium concentration detection by Fluo‐3/AM. RESULTS The calcium concentration were significantly increased in control group and NMDA group, and suppressed in PC group and MK‐801 group. The decrease of free calcium level by PC therapy was abolished by NMDA. CONCLUSION The ischemia postconditioning reduces the calcium overload through suppressing the activity of NMDA receptor.