花生四烯酸和溶血磷脂酰胆碱调节大鼠大脑皮质兴奋性递质氨基酸的释放。

Arachidonic acid and lysophosphatidylcholine modulate excitatory transmitter amino acid release from the rat cerebral cortex.

作者信息

O'Regan M H, Perkins L M, Phillis J W

机构信息

Department of Physiology, School of Medicine, Wayne State University, Detroit, MI 48201, USA.

出版信息

Neurosci Lett. 1995 Jun 30;193(2):85-8. doi: 10.1016/0304-3940(95)11672-j.

DOI:10.1016/0304-3940(95)11672-j

PMID:7478165

Abstract

The involvement of phospholipase A2 (PLA2) products in ischemia-evoked release of excitatory neurotransmitter amino acids (EAAs) from the cerebral cortex was studied in a four vessel occlusion rat model of cerebral ischemia/reperfusion. In comparison with untreated animals, arachidonic acid (AA; 5 x 10(-7) M to 5 x 10(-5) M) significantly reduced the ischemia-evoked efflux of glutamate and aspartate into cortical superfusates. Direct application of lysophosphatidylcholine (LysoPC; 55.4 micrograms/ml) to the cerebral cortex of non-ischemic animals resulted in a significant increase in glutamate levels. These results indicate that the immediate products of PLA2 action on plasma membrane phospholipids can either enhance or inhibit excitotoxic amino acid release following cerebral ischemia. The effect of AA is likely to be a result of its ability to inhibit PLA2; that of LysoPC, a consequence of its detergent action.

摘要

在大脑缺血/再灌注的四动脉闭塞大鼠模型中，研究了磷脂酶A2（PLA2）产物在缺血诱发的大脑皮质兴奋性神经递质氨基酸（EAA）释放中的作用。与未治疗的动物相比，花生四烯酸（AA；5×10^(-7) M至5×10^(-5) M）显著减少了缺血诱发的谷氨酸和天冬氨酸向皮质灌流液中的流出。将溶血磷脂酰胆碱（LysoPC；55.4微克/毫升）直接应用于非缺血动物的大脑皮质，导致谷氨酸水平显著升高。这些结果表明，PLA2作用于质膜磷脂的直接产物在脑缺血后既可以增强也可以抑制兴奋性毒性氨基酸的释放。AA的作用可能是其抑制PLA2能力的结果；LysoPC的作用则是其去污剂作用的结果。