稀释致死（dl）基因攻击小鼠浦肯野细胞树突棘中的钙储存。

The dilute-lethal (dl) gene attacks a Ca2+ store in the dendritic spine of Purkinje cells in mice.

作者信息

Takagishi Y, Oda S, Hayasaka S, Dekker-Ohno K, Shikata T, Inouye M, Yamamura H

机构信息

Research Institute of Environmental Medicine, Nagoya University, Japan.

出版信息

Neurosci Lett. 1996 Sep 13;215(3):169-72. doi: 10.1016/0304-3940(96)12967-0.

DOI:10.1016/0304-3940(96)12967-0

PMID:8899740

Abstract

The absence of smooth endoplasmic reticulum (SER) in the dendritic spine of Purkinje cells was found in dilute-lethal (dl) mouse cerebella as detected by immunohistochemistry using anti-inositol 1,4,5-triphosphate receptor antibody and electron microscopy. Since SER in the spine has been suggested to play a crucial role for synaptic regulation as an intracellular Ca2+ store (for reviews, see [Miller, R.J., Prog. Neurobiol., 37 (1991) 255-285: Simpson, P.B., Challiss, R.A.J. and Nahorski, S.R., Trends Neurosci., 18 (1995) 299-306]), a neurological defect, characterized by clonic convulsions with opisthotonus and ataxia, in the dilute-lethal mouse with homozygous trait may be attributable to the absence of SER in the dendritic spine of Purkinje cells.

摘要

利用抗肌醇1,4,5-三磷酸受体抗体进行免疫组织化学检测以及电子显微镜观察发现，在稀释致死（dl）小鼠的小脑浦肯野细胞树突棘中不存在光滑内质网（SER）。由于树突棘中的SER被认为作为细胞内钙库在突触调节中起关键作用（综述见[米勒，R.J.，《神经生物学进展》，37 (1991) 255 - 285；辛普森，P.B.，查利斯，R.A.J.和纳霍尔斯基，S.R.，《神经科学趋势》，18 (1995) 299 - 306]），具有纯合性状的稀释致死小鼠中以阵挛性惊厥伴角弓反张和共济失调为特征的神经缺陷可能归因于浦肯野细胞树突棘中SER的缺失。