THE NMDA RECEPTOR REDOX SITE CONTROLS NMDA-RECEPTOR-MEDIATED LONG-TERM POTENTIATION

被引：0
作者：
GOZLAN, H
DIABIRA, D
CHINESTRA, P
BENARI, Y
机构：
来源：
COMPTES RENDUS DE L ACADEMIE DES SCIENCES SERIE III-SCIENCES DE LA VIE-LIFE SCIENCES | 1994年 / 317卷 / 10期
关键词：
LONG-TERM POTENTIATION; NMDA RECEPTORS; AMPA RECEPTORS; ANOXIA; REDOX SITE;
D O I：
暂无
中图分类号：
Q [生物科学];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
In order to evaluate the role of the NMDA receptor redox site in long-term potentiation (LTP), we have investigated the effects of two redox reagents, 5,5'-dithiobis-2-nitrobenzoic acid (DTNB) and tris(carboxyethyl)phosphine (TCEP) on the induction and expression of various forms of LTP. DTNB a thiol-oxidizing agent, irreversibly reduces by 50% NMDA receptor EPSP. In the presence of DTNB, the induction of tetanic and anoxic LTP are prevented. When tetanic or anoxic LTP were generated first, DTNB completely reverses the potentiation and TCEP a disulfide-reducing agent restores LTP to its initial level. These redox agents have no effect on AMPA synaptic transmission and did not significantly modify the induction and the expression of tetanic AMPA-LTP. These results suggest that thiol-oxidizing compounds might be useful for the treatment of cerebral ischemia.
引用
收藏
页码：885 / 890
页数：6
相关论文
共 19 条
[1]   SELECTIVE MODULATION OF NMDA RESPONSES BY REDUCTION AND OXIDATION [J].
AIZENMAN, E ;
LIPTON, SA ;
LORING, RH .
NEURON, 1989, 2 (03) :1257-1263
[2]   THE RELATIVE CONTRIBUTION OF NMDA RECEPTOR CHANNELS IN THE EXPRESSION OF LONG-TERM POTENTIATION IN THE HIPPOCAMPAL CA1 REGION [J].
ASZTELY, F ;
WIGSTROM, H ;
GUSTAFSSON, B .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1992, 4 (08) :681-690
[3]   GALANIN AND GLIBENCLAMIDE MODULATE THE ANOXIC RELEASE OF GLUTAMATE IN RAT CA3 HIPPOCAMPAL-NEURONS [J].
BENARI, Y .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1990, 2 (01) :62-68
[4]   PROTEIN-KINASE-C MODULATION OF NMDA CURRENTS - AN IMPORTANT LINK FOR LTP INDUCTION [J].
BENARI, Y ;
ANIKSZTEJN, L ;
BREGESTOVSKI, P .
TRENDS IN NEUROSCIENCES, 1992, 15 (09) :333-339
[5]   SELECTIVE REDUCTION OF DISULFIDES BY TRIS(2-CARBOXYETHYL)PHOSPHINE [J].
BURNS, JA ;
BUTLER, JC ;
MORAN, J ;
WHITESIDES, GM .
JOURNAL OF ORGANIC CHEMISTRY, 1991, 56 (08) :2648-2650
[6]   A SELECTIVE LTP OF NMDA RECEPTOR-MEDIATED CURRENTS INDUCED BY ANOXIA IN CA1 HIPPOCAMPAL-NEURONS [J].
CREPEL, V ;
HAMMOND, C ;
CHINESTRA, P ;
DIABIRA, D ;
BENARI, Y .
JOURNAL OF NEUROPHYSIOLOGY, 1993, 70 (05) :2045-2055
[7]   EVIDENCE THAT THE LARGE LOSS OF GLUTATHIONE OBSERVED IN ISCHEMIA REPERFUSION OF THE SMALL-INTESTINE IS NOT DUE TO OXIDATION TO GLUTATHIONE DISULFIDE [J].
GIBSON, DD ;
BRACKETT, DJ ;
SQUIRES, RA ;
BALLA, AK ;
LERNER, MR ;
MCCAY, PB ;
PENNINGTON, LR .
FREE RADICAL BIOLOGY AND MEDICINE, 1993, 14 (04) :427-433
[8]   PYRIDINE-NUCLEOTIDE REDOX STATE AND BLOOD-FLOW OF CEREBRAL-CORTEX FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION IN CAT [J].
GINSBERG, MD ;
REIVICH, M ;
FRINAK, S ;
HARBIG, K .
STROKE, 1976, 7 (02) :125-131
[9]   NMDA RECEPTOR CHANNELS - SUBUNIT-SPECIFIC POTENTIATION BY REDUCING AGENTS [J].
KOHR, G ;
ECKARDT, S ;
LUDDENS, H ;
MONYER, H ;
SEEBURG, PH .
NEURON, 1994, 12 (05) :1031-1040
[10]   REGULATION OF THE NMDA RECEPTOR BY REDOX PHENOMENA - INHIBITORY ROLE OF ASCORBATE [J].
MAJEWSKA, MD ;
BELL, JA ;
LONDON, ED .
BRAIN RESEARCH, 1990, 537 (1-2) :328-332
12