体外缺氧对突触体中去极化刺激的肌醇磷酸积累的影响。

Effects of in vitro hypoxia on depolarization-stimulated accumulation of inositol phosphates in synaptosomes.

作者信息

Huang H M, Gibson G E

机构信息

Cornell University Medical College, Burke Rehabilitation Center, White Plains, NY 10605.

出版信息

Life Sci. 1989;45(16):1443-9. doi: 10.1016/0024-3205(89)90034-9.

DOI:10.1016/0024-3205(89)90034-9

PMID:2811601

Abstract

The effects of potassium and in vitro histotoxic hypoxia (i.e. KCN) on phosphatidylinositol turnover in rat cortical synaptosomes were determined. [2-3H] Inositol prelabelled rat synaptosomes were prepared from cerebral cortex slices that had been incubated with [2-3H] inositol. Depolarization with 60 mM KCl increased [2-3H] inositol phosphates in a time dependent manner. Depolarization with 60 mM KCl increased [2-3H] inositol trisphosphate transiently at 5 s. K+ induced rapid formation of [2-3H]-inositol bisphosphate and maintained an elevated level for at least 5 min. K+ stimulated gradual formation of [2-3H] inositol monophosphate with time. One minute of hypoxia enhanced potassium-stimulated [2-3H] inositol bisphosphate formation. However, 30 min of hypoxia impaired potassium-stimulated accumulation of [2-3H] inositol phosphates. The effects of histotoxic hypoxia were all dependent upon calcium in the medium and on K+-depolarization. Thus, hypoxia altered the K+-induced accumulation of inositol phosphates in prelabelled synaptosomes in a time dependent, biphasic manner that was calcium dependent.

摘要

测定了钾和体外组织毒性缺氧（即KCN）对大鼠皮质突触体中磷脂酰肌醇代谢的影响。用[2-³H]肌醇预标记的大鼠突触体是由与[2-³H]肌醇孵育过的大脑皮质切片制备而来。用60 mM KCl进行去极化以时间依赖的方式增加了[2-³H]肌醇磷酸。用60 mM KCl进行去极化在5 s时短暂增加了[2-³H]肌醇三磷酸。钾诱导了[2-³H]肌醇二磷酸的快速形成，并使其水平至少维持升高5分钟。随着时间的推移，钾刺激了[2-³H]肌醇单磷酸的逐渐形成。1分钟的缺氧增强了钾刺激的[2-³H]肌醇二磷酸的形成。然而，30分钟的缺氧损害了钾刺激的[2-³H]肌醇磷酸的积累。组织毒性缺氧的影响均依赖于培养基中的钙和钾去极化。因此，缺氧以时间依赖的双相方式改变了预标记突触体中钾诱导的肌醇磷酸积累，且这种改变依赖于钙。