Extracellular levels of quinolinic acid are moderately increased in rat neostriatum following severe insulin-induced hypoglycaemia.
Extracellular levels of quinolinic acid are moderately increased in rat neostriatum following severe insulin-induced hypoglycaemia.
复制标题
严重胰岛素引起的低血糖后，大鼠新纹状体中喹啉酸的细胞外水平中度升高。
DOI：
10.1111/j.1748-1716.1990.tb08865.x
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Schwarcz,R
中科院分区：
文献类型：
--
作者：
Westerberg,E;Magnusson,K;Wieloch,T;Ungerstedt,U;Speciale,C;Schwarcz,R
在胰岛素诱导的低血糖30分钟期间和之后，通过微透析监测大鼠新纹状体和海马/皮质中脑代谢物喹啉酸（一种内源性兴奋毒素）的细胞外浓度。在低血糖诱导的等电期间，纹状体中喹啉酸的细胞外水平（基础值，1.1± 0.3 pmol/30 μl部分）与对照期相比升高1.7倍。低血糖后30至90分钟，观察到细胞外喹啉酸显著增加至基础水平的2.2倍。恢复2 h后，在背外侧纹状体观察到神经元坏死的开始。透析探针的植入不影响神经元损伤的程度。在海马/cortic.The数据表明，严重的低血糖损伤后，脆弱的纹状体细胞暴露于超生理的细胞外喹啉酸浓度在一段较长的时间没有观察到细胞外喹啉酸水平的变化。考虑到大鼠纹状体神经元对毒素的明显敏感性，喹啉酸细胞外水平的小而长时间的升高可能对低血糖中迟发性神经元死亡的发展具有重要意义。
Extracellular concentrations of the brain metabolite quinolinic acid, an endogenous excitotoxin, were monitored by microdialysis in rat neostriatum and hippocampus/cortex during and following a 30‐min period of insulin‐induced hypoglycaemia. During hypoglycaemia‐induced isoelectricity, extracellular levels of quinolinic acid in the striatum (basal value, 1.1±0.3pmol per 30‐μl fraction) were elevated 1.7 times as compared to the control period. Thirty to ninety minutes following hypoglycaemia a significant increase in extracellular quinolinic acid to 2.2 times basal level was noted. After 2 h recovery, the beginning of neuronal necrosis was observed in the dorsolateral striatum. Implantation of the dialysis probe did not influence the extent of neuronal damage. No changes in extracellular quinolinic acid levels were observed in the hippocampus/cortex.The data indicate that following a severe hypoglycaemic insult vulnerable striatal cells are exposed to hyperphysiological extracellular quinolinic acid concentrations over an extended period of time. Considering the pronounced susceptibility of rat striatal neurons to the toxin, the small but prolonged elevation in the extracellular levels of quinolinic acid could be of significance for the development of delayed neuronal death in hypoglycaemia.