甘氨酸通过不同机制在缺血性损伤中发挥双重作用

Department of Neurobiology, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China

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. © 2012 American Heart Association, Inc.

Lu, W.; Department of Neurobiology, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China; email: lu@njmu.edu.cn