Relationship between the activation of cyclic AMP responsive element binding protein and ischemic tolerance in the penumbra region of rat cerebral cortex

被引:33
作者
Nakajima, T
Iwabuchi, S
Miyazaki, H
Okuma, Y
Inanami, O
Kuwabara, M
Nomura, Y
Kawahara, K [1 ]
机构
[1] Hokkaido Univ, Lab Biomed Control, Res Inst Elect Sci, Sapporo, Hokkaido 0600812, Japan
[2] Hokkaido Univ, Dept Pharmacol, Grad Sch Pharmaceut Sci, Sapporo, Hokkaido 0600812, Japan
[3] Hokkaido Univ, Radiat Biol Lab, Dept Environm Vet Sci, Grad Sch Vet Med, Sapporo, Hokkaido 0600812, Japan
关键词
ischemic tolerance; cyclic AMP responsive element binding protein; focal cerebral ischemia;
D O I
10.1016/S0304-3940(02)00752-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Application of a brief period of ischemia, i.e. preconditioning treatment of the middle cerebral artery territory, has been known to produce ischemic tolerance, reducing cerebral infarction volume in the penumbra region after lethal ischemia. However, little is known about the molecular mechanisms responsible for preconditioning-induced ischemic tolerance. In the present study, we examined the difference in the phosphorylation pattern of cyclic AMP responsive element binding protein (CREB) after 1 h of focal cerebral ischemia between preconditioned and non-preconditioned rats by immunohistochemistry and Western blotting. The phosphorylation of CREB in the penumbra region was more rapidly enhanced in the preconditioned rats than in the non-preconditioned rats after 1 h of ischemia. The result suggested that the immediate enhancement in the phosphorylation of CREB in the penumbra region prevented the spread of infarction in the preconditioned rats. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:13 / 16
页数:4
相关论文
共 20 条
[11]   CORRELATION BETWEEN CEREBRAL BLOOD-FLOW AND HISTOLOGIC-CHANGES IN A NEW RAT MODEL OF MIDDLE CEREBRAL-ARTERY OCCLUSION [J].
NAGASAWA, H ;
KOGURE, K .
STROKE, 1989, 20 (08) :1037-1043
[12]  
STANGLIANO NE, 1999, J CEREB BLOOD FLOW M, V19, P757
[13]   Temporal profile of CREB phosphorylation after focal ischemia in rat brain [J].
Tanaka, K ;
Nogawa, S ;
Nagata, E ;
Suzuki, S ;
Dembo, T ;
Kosakai, A ;
Fukuuchi, Y .
NEUROREPORT, 1999, 10 (11) :2245-2250
[14]   Induction of ischemic tolerance and antioxidant activity by brief focal ischemia [J].
Toyoda, T ;
Kassell, NF ;
Lee, KS .
NEUROREPORT, 1997, 8 (04) :847-851
[15]  
Walton M, 1999, J NEUROCHEM, V73, P1836
[16]   Is CREB a key to neuronal survival? [J].
Walton, MR ;
Dragunow, M .
TRENDS IN NEUROSCIENCES, 2000, 23 (02) :48-53
[17]  
Wilson BE, 1996, MOL CELL BIOL, V16, P5546
[18]   Three-vessel occlusion using a micro-clip for the proximal left middle cerebral artery produces a reliable neocortical infarct in rats [J].
Yanamoto, H ;
Nagata, I ;
Hashimoto, N ;
Kikuchi, H .
BRAIN RESEARCH PROTOCOLS, 1998, 3 (02) :209-220
[19]   DNA fragmentation in ischemic core and penumbra in focal cerebral ischemia in rats [J].
Yao, H ;
Takasawa, R ;
Fukuda, K ;
Shiokawa, D ;
Sadanaga-Akiyoshi, F ;
Ibayashi, S ;
Tanuma, S ;
Uchimura, H .
MOLECULAR BRAIN RESEARCH, 2001, 91 (1-2) :112-118
[20]   AMPA receptor-mediated, calcium-dependent CREB phosphorylation in a subpopulation of auditory neurons surviving activity deprivation [J].
Zirpel, L ;
Janowiak, MA ;
Veltri, CA ;
Parks, TN .
JOURNAL OF NEUROSCIENCE, 2000, 20 (16) :6267-6275