氧化磷酸化解偶联过程中完整神经元线粒体中环孢菌素A敏感孔的诱导。

Induction of cyclosporin A-sensitive pore in mitochondria of intact neurons during uncoupling of oxidative phosphorylation.

作者信息

Storozhevykh T P, Yuryavichyus A I, Sorokina E G, Pinelis V G

机构信息

Laboratory of Membranology, Center of Children Health, Russian Academy of Medical Sciences, Moscow.

出版信息

Bull Exp Biol Med. 2001 May;131(5):440-3. doi: 10.1023/a:1017963629229.

DOI:10.1023/a:1017963629229

PMID:11550047

Abstract

Using primary cultures of cerebellar granule cells we showed that Ca(2+)transported into neurons under the effect of glutamate is accumulated and stored in mitochondria for a long time. Protonophore FCCP, an uncoupler of oxidative phosphorylation, stimulated the release of Ca(2+)from mitochondria in a calcium-free medium in 81% glutamate-treated cells. Cyclosporin A and ATP-synthase blocker oligomycin decreased the number of cells with FCCP-induced Ca(2+)release to 53 and 12%, respectively. Oligomycin partly prevented glutamate- and FCCP-induced decrease of intracellular ATP level.

摘要

利用小脑颗粒细胞的原代培养物，我们发现，在谷氨酸作用下转运到神经元内的Ca(2+)会长期积累并储存在线粒体中。氧化磷酸化解偶联剂质子载体FCCP在无钙培养基中刺激了81%经谷氨酸处理的细胞中线粒体释放Ca(2+)。环孢菌素A和ATP合酶抑制剂寡霉素分别将FCCP诱导的Ca(2+)释放的细胞数量降至53%和12%。寡霉素部分阻止了谷氨酸和FCCP诱导的细胞内ATP水平的降低。