Heat-shock pretreatment prevents suppression of long-term potentiation induced by scopolamine in rat hippocampal CA1 synapses

被引:18
作者
Lin, YW
Yang, HW
Min, MY
Chiu, TH [1 ]
机构
[1] Natl Yang Ming Univ, Dept Physiol, Taipei 112, Taiwan
[2] Chung Shan Med Univ, Dept Life Sci, Taichung 406, Taiwan
[3] Chinese Med Coll, Dept Physiol, Taichung 404, Taiwan
关键词
long-term potentiation; scopolamine; heat shock; hippocampus;
D O I
10.1016/j.brainres.2003.11.057
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We examined the effect of heat-shock pretreatment on long-term potentiation (LTP) in the CA1 hippocampal slices of the rat using the muscarinic blocker scopolamine as the UP (memory) suppressor. Time course study using immunohistochemical techniques indicated peak expression of HSP70 16 h after heat-shock treatment. Focusing on that time point we found tetanic stimulation (at 100 Hz) induced LTP of 191.1 +/- 12.2% in control slices (n = 7), which was suppressed by scopolamine to 114.5 +/- 2.8 %. Heat-shock pretreatment successfully prevented such suppression (216.6 +/- 38.2%, and 190.2 +/- 10.6% with and without scopolamine, respectively, n = 7). Both HSP expression and LTP responses were relatively small taken either 2 or 48 h after heat-shock or sham pretreatment. These results suggest that the induction of HSPs is time-dependent and can prevent scopolamine-mediated UP suppression. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:222 / 226
页数:5
相关论文
共 20 条
[1]   DISSOCIATION OF HSP70 AND HSC70 HEAT-SHOCK MESSENGER-RNA INDUCTIONS AS AN EARLY BIOCHEMICAL MARKER OF ISCHEMIC NEURONAL DEATH [J].
ABE, K ;
KAWAGOE, J ;
AOKI, M ;
KOGURE, K .
NEUROSCIENCE LETTERS, 1993, 149 (02) :165-168
[2]   LONG-LASTING POTENTIATION OF SYNAPTIC TRANSMISSION IN DENTATE AREA OF ANESTHETIZED RABBIT FOLLOWING STIMULATION OF PERFORANT PATH [J].
BLISS, TVP ;
LOMO, T .
JOURNAL OF PHYSIOLOGY-LONDON, 1973, 232 (02) :331-356
[3]   A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS [J].
BLISS, TVP ;
COLLINGRIDGE, GL .
NATURE, 1993, 361 (6407) :31-39
[4]   Activation of M1-like muscarinic receptors is required for the induction of corticostriatal LTP [J].
Calabresi, P ;
Centonze, D ;
Gubellini, P ;
Bernardi, G .
NEUROPHARMACOLOGY, 1999, 38 (02) :323-326
[5]   EXPRESSION OF HEAT-SHOCK PROTEINS IN ALZHEIMERS-DISEASE [J].
HAMOS, JE ;
OBLAS, B ;
PULASKISALO, D ;
WELCH, WJ ;
BOLE, DG ;
DRACHMAN, DA .
NEUROLOGY, 1991, 41 (03) :345-350
[6]   Heat shock proteins and cardiac protection [J].
Latchman, DS .
CARDIOVASCULAR RESEARCH, 2001, 51 (04) :637-646
[7]  
Lin YW, 2003, J NEUROSCI, V23, P4173
[8]   Heat shock prevents simulated ischemia-induced apoptosis in renal tubular cells via a PKC-dependent mechanism [J].
Meldrum, KK ;
Meldrum, DR ;
Sezen, SF ;
Crone, JK ;
Burnett, AL .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2001, 281 (01) :R359-R364
[9]   Long-term potentiation and dual-component quantal signaling in the dentate gyrus [J].
Min, MY ;
Asztely, F ;
Kokaia, M ;
Kullmann, DM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (08) :4702-4707
[10]   KAINIC ACID-INDUCED HEAT-SHOCK PROTEIN-70, MESSENGER-RNA AND PROTEIN EXPRESSION IS INHIBITED BY MK-801 IN CERTAIN RAT-BRAIN REGIONS [J].
PLANAS, AM ;
SORIANO, MA ;
FERRER, I ;
FARRE, ER .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1995, 7 (02) :293-304