钙蛋白酶可能在长时程增强中产生一种不依赖钙离子的蛋白激酶C形式。

Calpain may produce a Ca(2+)-independent form of kinase C in long-term potentiation.

作者信息

Suzuki T, Okumura-Noji K, Ogura A, Tanaka R, Nakamura K, Kudo Y

机构信息

Department of Biochemisry, Nagoya City University Medical School, Japan.

出版信息

Biochem Biophys Res Commun. 1992 Dec 30;189(3):1515-20. doi: 10.1016/0006-291x(92)90247-i.

DOI:10.1016/0006-291x(92)90247-i

PMID:1482363

Abstract

Both an enhancement of Ca(2+)-independent kinase activity in the supernatant fraction and enhanced breakdown of type beta kinase C (PKC-beta) were observed in the hippocampus after induction of tetanus-induced long-term potentiation (LTP) in the hippocampal CA1 region of rat. The enhanced activity was inhibited by the PKC-specific inhibitor, PKC19-36. Both phenomena were also observed simultaneously in the in vitro model system in which hippocampal homogenate was treated with CaCl2, and both enhancements were inhibited by the addition of calpain inhibitors, leupeptin and benzyloxycarbonyl-Leu-Met-H. The results suggest that Ca(2+)-independent kinase activity enhanced in the supernatant fraction during LTP derives from the catalytic fragment of PKC-beta released by calpain.

摘要

在大鼠海马CA1区诱导破伤风诱导的长时程增强（LTP）后，海马体中观察到上清液部分Ca（2+）非依赖性激酶活性增强，以及β型蛋白激酶C（PKC-β）的分解增强。PKC特异性抑制剂PKC19-36可抑制增强的活性。在用CaCl2处理海马匀浆的体外模型系统中也同时观察到了这两种现象，并且通过添加钙蛋白酶抑制剂亮抑酶肽和苄氧羰基-Leu-Met-H可抑制这两种增强作用。结果表明，LTP期间上清液部分增强的Ca（2+）非依赖性激酶活性源自钙蛋白酶释放的PKC-β催化片段。