溶血磷脂酸对突触体（Na⁺ + K⁺）-ATP酶活性的抑制作用：其在膜去极化中的可能作用。

Inhibition of synaptosomal (Na+ + K+)-ATPase activity by lysophosphatidic acid: its possible role in membrane depolarization.

作者信息

Nishikawa T, Tomori Y, Yamashita S, Shimizu S

机构信息

Department of Pharmacology, Kagoshima University Dental School, Japan.

出版信息

Jpn J Pharmacol. 1988 Jun;47(2):143-50. doi: 10.1254/jjp.47.143.

DOI:10.1254/jjp.47.143

PMID:2848959

Abstract

Lysophosphatidic acid (LPA), a metabolite of phosphatidic acid (PA) by phospholipases of the A2 type, markedly inhibited the synaptic membrane (Na+ + K+)-ATPase activity from rat cerebral cortices in incubation media containing free Ca2+ concentrations below 4.7 x 10(-6) M. This effect of LPA was dose-dependent, and the minimum effective concentration was 10(-6) g/ml. The inhibitory action of LPA was more potent than that of PA. Lysophosphatidylinositol (LPI) and lysophosphatidylethanolamine (LPE) at 10(-5) g/ml had little or no effect on this enzyme activity. These results suggest that LPA may partly play a role in the depolarization and/or increase in intracellular calcium concentrations in the brain.

摘要

溶血磷脂酸（LPA）是磷脂酸（PA）经A2型磷脂酶代谢产生的产物，在游离钙离子浓度低于4.7×10⁻⁶ M的孵育介质中，它能显著抑制大鼠大脑皮质突触膜（Na⁺ + K⁺）-ATP酶的活性。LPA的这种作用呈剂量依赖性，最小有效浓度为10⁻⁶ g/ml。LPA的抑制作用比PA更强。10⁻⁵ g/ml的溶血磷脂酰肌醇（LPI）和溶血磷脂酰乙醇胺（LPE）对该酶活性几乎没有影响。这些结果表明，LPA可能在大脑去极化和/或细胞内钙浓度升高中发挥部分作用。