Journal
STROKE
Volume 43, Issue 8, Pages 2212-U390Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/STROKEAHA.111.645994
Keywords
glycine; ischemia; electrophysiology; middle cerebral artery occlusion; N-methyl-D; aspartate receptor
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Funding
- National Natural Science Foundation of China (NFSC) [31025011, 30970934]
- Major State Basic Research Program of China [2010CB912002]
- Education Department of Jiangsu Province [08KJA180004]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- State Key Laboratory of Bioelectronics, Southeast University
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Background and Purpose-We characterized the differential effects of glycine at different levels in the induction of postischemic long-term potentiation, as well as in the neuronal damage induced by focal ischemia. Methods-Whole-cell patch clamp recordings were obtained from rat hippocampal slice preparations. In vitro ischemia and postischemic long-term potentiation were induced by oxygen and glucose deprivation. In vivo ischemia was induced by transient middle cerebral artery occlusion. Results-In both in vitro and in vivo ischemia models, glycine at low level exerts deleterious effects in postischemic long-term potentiation and ischemic neuronal injury by modulation of the N-methyl-D-aspartate receptor coagonist site; whereas glycine at high level exerts neuroprotective effects by activation of glycine receptor and subsequent differential regulation of N-methyl-D-aspartate receptor subunit components. Conclusions-Our results provide a molecular basis for the dual roles of glycine in ischemic injury through distinct mechanisms, and they suggest that glycine receptors could be a potential target for clinical treatment of stroke. (Stroke. 2012; 43: 2212-2220.)
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