缺氧低血糖诱导的猴海马切片中温度依赖性Ca2+动员

Temperature-dependent Ca2+ mobilization induced by hypoxia-hypoglycemia in the monkey hippocampal slices.

作者信息

Yamashima T, Takita M, Akaike S, Hirano M, Miyakawa A, Miyazawa A, Kudo Y, Yoshioka T

机构信息

Dept. of Neurosurgery, Kanazawa Univ. School of Medicine, Japan.

出版信息

Biochem Biophys Res Commun. 1994 Dec 30;205(3):1843-9. doi: 10.1006/bbrc.1994.2885.

DOI:10.1006/bbrc.1994.2885

PMID:7811273

Abstract

Mobilization of [Ca2+]i in the monkey hippocampal slices during transient hypoxia-hypoglycemia and KCl-induced depolarization was analyzed by microfluorometric imaging and anti-PIP2 immunohistochemistry. Hypoxia-hypoglycemia provoked the largest [Ca2+]i mobilization of CA-1 temperature-dependently whereas [Ca2+]i mobilization by KCl-induced depolarization occurred independent of the temperature in CA-2. Immunohistochemical analysis of the hippocampus after hypoxia-hypoglycemia showed an increased PIP2 staining preferentially in the perikarya of CA-1 neurons. These data suggest that release of Ca2+ from intracellular stores caused by PIP2 breakdown may induce elevated [Ca2+]i.

摘要

通过显微荧光成像和抗磷脂酰肌醇-4,5-二磷酸（PIP2）免疫组织化学分析，研究了短暂性缺氧-低血糖和氯化钾诱导的去极化过程中，猴海马切片中细胞内钙离子浓度（[Ca2+]i）的动员情况。缺氧-低血糖以温度依赖的方式引起CA-1区最大程度的[Ca2+]i动员，而氯化钾诱导的去极化引起的[Ca2+]i动员在CA-2区与温度无关。缺氧-低血糖后海马的免疫组织化学分析显示，PIP2染色增加，且优先出现在CA-1神经元的胞体周围。这些数据表明，PIP2分解导致细胞内钙库释放Ca2+可能诱导[Ca2+]i升高。