Up-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats

被引：11

作者：

Cao, Fang ^{[1
]}

Hata, Ryuji ^{[1
]}

Zhu, Pengxiang ^{[1
]}

Niinobe, Michinobu ^{[2
]}

Sakanaka, Masahiro ^{[1
]}

机构：

[1] Ehime Univ, Grad Sch Med, Dept Funct Histol, Toon, Ehime 7910295, Japan

[2] Osaka Univ, Inst Prot Res, Div Regulat Macromol Funct, Suita, Osaka 5650871, Japan

来源：

BRAIN RESEARCH | 2009年 / 1272卷

关键词：

SNARE; Cerebral ischemia; Synaptotagmin; SYNAPTOTAGMIN-I; CA2+ SENSOR; MICROGLIA; DEATH; TERMINALS; RELEASE; FUSION; DAMAGE; NMDA; AMPA;

D O I：

10.1016/j.brainres.2009.03.047

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Syntaxin1 and synaptotagmin are located in the pre-synaptic terminals and play central roles in Ca2+-triggered neurotransmitter release. Because excessive synaptic transmission has been implicated in neuronal cell death after ischemia, we investigated the effects of cerebral ischemia on the levels of these proteins using a rat permanent focal ischemia model. Western blot analysis revealed that the protein level of syntaxin1 was significantly up-regulated in the ischemic core cortex and peri-ischemic cortex at 1 day after ischemia, while the protein level of synaptotagmin was not. Immunohistochemical analysis revealed that the protein level of syntaxin1 was markedly up-regulated in the ischemic areas where immunoreaction for MAP2 was lost. Furthermore, we showed that resident microglial cells were quite vulnerable to ischemia. Our data provide novel insights into the molecular mechanism of cerebral ischemia at the pre-synaptic terminals. (C) 2009 Elsevier B.V. All rights reserved.

引用

页码：52 / 61

页数：10

共 36 条

[1] Isolation and characterization of BART-1: A novel balloon angioplasty responsive transcript in rat carotid arteries [J].

Autieri, MV ;

Prystowsky, MB ;

Ohlstein, EH .

DNA AND CELL BIOLOGY, 1996, 15 (04) :297-304

[2] Effect of hyperbaric oxygen on striatal metabolites: a microdialysis study in awake freely moving rats after MCA occlusion [J].

Badr, AE ;

Yin, W ;

Mychaskiw, G ;

Zhang, JH .

BRAIN RESEARCH, 2001, 916 (1-2) :85-90

[3] Fusion pore dynamics are regulated by synaptotagmin•t-SNARE interactions [J].

Bai, JH ;

Wang, CT ;

Richards, DA ;

Jackson, MB ;

Chapman, ER .

NEURON, 2004, 41 (06) :929-942

[4] Evidence that syntaxin 1A is involved in storage in the secretory pathway [J].

Bittner, MA ;

Bennett, MK ;

Holz, RW .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (19) :11214-11221

[5] INHIBITION OF NEUROTRANSMITTER RELEASE BY C2-DOMAIN PEPTIDES IMPLICATES SYNAPTOTAGMIN IN EXOCYTOSIS [J].

BOMMERT, K ;

CHARLTON, MP ;

DEBELLO, WM ;

CHIN, GJ ;

BETZ, H ;

AUGUSTINE, GJ .

NATURE, 1993, 363 (6425) :163-165

[6] How does synaptotagmin trigger neurotransmitter release? [J].

Chapman, Edwin R. .

ANNUAL REVIEW OF BIOCHEMISTRY, 2008, 77 :615-641

[7] 17β-estradiol treatment following permanent focal ischemia does not influence recovery of sensorimotor function [J].

Farr, Tracy D. ;

Carswell, Hilary V. O. ;

Gallagher, Lindsay ;

Condon, Barrie ;

Fagan, Andrew J. ;

Mullin, Jim ;

Macrae, I. Mhairi .

NEUROBIOLOGY OF DISEASE, 2006, 23 (03) :552-562

[8] SYNAPTOTAGMIN-I - A MAJOR CA2+ SENSOR FOR TRANSMITTER RELEASE AT A CENTRAL SYNAPSE [J].

GEPPERT, M ;

GODA, Y ;

HAMMER, RE ;

LI, C ;

ROSAHL, TW ;

STEVENS, CF ;

SUDHOF, TC .

CELL, 1994, 79 (04) :717-727

[9] Cerebral preconditioning and ischaemic tolerance [J].

Gidday, Jeffrey M. .

NATURE REVIEWS NEUROSCIENCE, 2006, 7 (06) :437-448

[10] Immunosuppression after traumatic or ischemic CNS damage: It is neuroprotective and illuminates the role of microglial cells [J].

Hailer, Nils P. .

PROGRESS IN NEUROBIOLOGY, 2008, 84 (03) :211-233

← 1 2 3 4 →