Upregulation of GluR2 decreases intracellular Ca2+ following ischemia in developing gerbils

被引:13
作者
Oguro, K [1 ]
Miyawaki, T
Yokota, H
Kato, K
Kamiya, T
Katayama, Y
Fukaya, M
Watanabe, M
Shimazaki, K
机构
[1] Jichi Med Sch, Dept Neurol Surg, Minami Kawachi, Tochigi 3290498, Japan
[2] Jichi Med Sch, Dept Physiol, Minami Kawachi, Tochigi 3290498, Japan
[3] Nippon Med Coll, Dept Internal Med 2, Tokyo 113, Japan
[4] Hokkaido Univ, Sch Med, Sapporo, Hokkaido 060, Japan
关键词
ischemia; calcium; hippocampus; resistance; developing gerbils;
D O I
10.1016/j.neulet.2004.03.091
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Developing animals are known to be resistant to cerebral ischemia. To investigate the mechanisms by which developing animals exhibit ischemic resistance, we examined the changes in intracellular calcium ([Ca2+](i)) after oxygen-glucose deprivation (OGD) using hippocampal slices from gerbils. We found that increases of [Ca2+](i) in hippocampal CA1 neurons is significantly less after OGD in developing gerbils than in adults. Western blot analysis of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) receptors (AMPARs) showed that GluR2 expression, but not that of the other AMPARs is significantly higher in developing gerbils than in adults. Expression of the anti-apoptotic proteins such as HSP70, Bcl-X-L, and plasma membrane Ca2+-ATPase type1 (PMCA1) are not higher in the developing gerbils than in adults. These results suggest that the higher expression of GluR2 is important for the smaller increases in [Ca2+](i) and enhanced resistance to ischemia-induced neuronal damage in developing animals. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:101 / 105
页数:5
相关论文
共 20 条
[1]   CHANGES OF MITOCHONDRIAL-DNA AND HEAT-SHOCK PROTEIN GENE EXPRESSIONS IN GERBIL HIPPOCAMPUS AFTER TRANSIENT FOREBRAIN ISCHEMIA [J].
ABE, K ;
KAWAGOE, J ;
AOKI, M ;
KOGURE, K .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (05) :773-780
[2]   ACCELERATION OF HSP70 AND HSC70 HEAT-SHOCK GENE-EXPRESSION FOLLOWING TRANSIENT ISCHEMIA IN THE PRECONDITIONED GERBIL HIPPOCAMPUS [J].
AOKI, M ;
ABE, K ;
KAWAGOE, J ;
NAKAMURA, S ;
KOGURE, K .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (05) :781-788
[3]  
DALDERONE A, 2003, J NEUROSCI, V23, P2112
[4]   Bcl-2, Bax and Bcl-x expression following hypoxia-ischemia in the infant rat brain [J].
Ferrer, I ;
Pozas, E ;
Lopez, E ;
Ballabriga, J .
ACTA NEUROPATHOLOGICA, 1997, 94 (06) :583-589
[5]  
FRIEDMAN LK, 1994, J NEUROSCI, V14, P2697
[6]   Nitric oxide mediates cerebral ischemic tolerance in a neonatal rat model of hypoxic preconditioning [J].
Gidday, JM ;
Shah, AR ;
Maceren, RG ;
Wang, QO ;
Pelligrino, DA ;
Holtzman, DM ;
Park, TS .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (03) :331-340
[7]   Status epilepticus decreases glutamate receptor 2 mRNA and protein expression in hippocampal pyramidal cells before neuronal death [J].
Grooms, SY ;
Opitz, T ;
Bennett, MVL ;
Zukin, RS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (07) :3631-3636
[8]   CA2+ PERMEABILITY OF KA-AMPA GATED GLUTAMATE RECEPTOR CHANNELS DEPENDS ON SUBUNIT COMPOSITION [J].
HOLLMANN, M ;
HARTLEY, M ;
HEINEMANN, S .
SCIENCE, 1991, 252 (5007) :851-853
[9]   ISCHEMIC TOLERANCE PHENOMENON DETECTED IN VARIOUS BRAIN-REGIONS [J].
KITAGAWA, K ;
MATSUMOTO, M ;
KUWABARA, K ;
TAGAYA, M ;
OHTSUKI, T ;
HATA, R ;
UEDA, H ;
HANDA, N ;
KIMURA, K ;
KAMADA, T .
BRAIN RESEARCH, 1991, 561 (02) :203-211
[10]   ISCHEMIC TOLERANCE PHENOMENON FOUND IN THE BRAIN [J].
KITAGAWA, K ;
MATSUMOTO, M ;
TAGAYA, M ;
HATA, R ;
UEDA, H ;
NIINOBE, M ;
HANDA, N ;
FUKUNAGA, R ;
KIMURA, K ;
MIKOSHIBA, K ;
KAMADA, T .
BRAIN RESEARCH, 1990, 528 (01) :21-24