Nicotine modulates the neurotoxic effect of beta-amyloid protein((25-35)) in hippocampal cultures

被引：72

作者：

Zamani, MR ^{[1
]}

Allen, YS ^{[1
]}

Owen, GP ^{[1
]}

Gray, JA ^{[1
]}

机构：

[1] INST PSYCHIAT,DEPT PSYCHOL,LONDON SE5 8AF,ENGLAND

来源：

NEUROREPORT | 1997年 / 8卷 / 02期

基金：

英国惠康基金;

关键词：

beta AP((25-35)); mecamylamine; neuroprotection; neurotoxicity; nicotine; rat hippocampus;

D O I：

10.1097/00001756-199701200-00027

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

TWO major features of Alzheimer's disease (AD) are beta-amyloid protein (beta AP) deposition and a severe cholinergic deficit. An association between the two is suggested by the negative correlation found between cigarette smoking and AD. We sought to investigate this further by examining the effects of acute and chronic nicotine exposure on beta AP-induced neuronal loss in rat hippocampal cultures. Nicotine was found to attenuate the neurotoxicity of higher concentrations of beta AP((25-35)), an effect which was enhanced by longer nicotine pretreatment and significantly inhibited by the nicotine receptor antagonist mecamylamine. Our results suggest that nicotine partially protects against the neurotoxic actions of beta AP((25-35)) via a receptor-mediated pathway.

引用

收藏

页码：513 / 517

页数：5

相关论文

共 30 条

[1] NICOTINE-INDUCED PROTECTION OF CULTURED CORTICAL-NEURONS AGAINST N-METHYL-D-ASPARTATE RECEPTOR-MEDIATED GLUTAMATE CYTOTOXICITY [J].

AKAIKE, A ;

TAMURA, Y ;

YOKOTA, T ;

SHIMOHAMA, S ;

KIMURA, J .

BRAIN RESEARCH, 1994, 644 (02) :181-187

[2]

ALKONDON M, 1992, MOL PHARMACOL, V41, P802

[3]

ALKONDON M, 1993, J PHARMACOL EXP THER, V265, P1455

[4] BETA-AMYLOID CA2+-CHANNEL HYPOTHESIS FOR NEURONAL DEATH IN ALZHEIMER-DISEASE [J].

ARISPE, N ;

POLLARD, HB ;

ROJAS, E .

MOLECULAR AND CELLULAR BIOCHEMISTRY, 1994, 140 (02) :119-125

[5] ALPHA-BUNGAROTOXIN BINDING-SITES IN RAT HIPPOCAMPAL AND CORTICAL CULTURES - INITIAL CHARACTERIZATION, COLOCALIZATION WITH ALPHA-7 SUBUNITS AND UP-REGULATION BY CHRONIC NICOTINE TREATMENT [J].

BARRANTES, GE ;

ROGERS, AT ;

LINDSTROM, J ;

WONNACOTT, S .

BRAIN RESEARCH, 1995, 672 (1-2) :228-236

[6] NICOTINE ENHANCES 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE NEUROTOXICITY [J].

BEHMAND, RA ;

HARIK, SI .

JOURNAL OF NEUROCHEMISTRY, 1992, 58 (02) :776-779

[7] A CASE-CONTROL STUDY OF TWIN PAIRS DISCORDANT FOR PARKINSONS-DISEASE - A SEARCH FOR ENVIRONMENTAL RISK-FACTORS [J].

BHARUCHA, NE ;

STOKES, L ;

SCHOENBERG, BS ;

WARD, C ;

INCE, S ;

NUTT, JG ;

ELDRIDGE, R ;

CALNE, DB ;

MANTEL, N ;

DUVOISIN, R .

NEUROLOGY, 1986, 36 (02) :284-288

[8] THE CA2+ INFLUX INDUCED BY BETA-AMYLOID PEPTIDE-25-35 IN CULTURED HIPPOCAMPAL-NEURONS RESULTS FROM NETWORK EXCITATION [J].

BRORSON, JR ;

BINDOKAS, VP ;

IWAMA, T ;

MARCUCCILLI, CJ ;

CHISHOLM, JC ;

MILLER, RJ .

JOURNAL OF NEUROBIOLOGY, 1995, 26 (03) :325-338

[9] PATHOLOGICAL-CHANGES IN THE NUCLEUS OF MEYNERT IN ALZHEIMERS AND PARKINSONS DISEASES [J].

CANDY, JM ;

PERRY, RH ;

PERRY, EK ;

IRVING, D ;

BLESSED, G ;

FAIRBAIRN, AF ;

TOMLINSON, BE .

JOURNAL OF THE NEUROLOGICAL SCIENCES, 1983, 59 (02) :277-289

[10] AN AMYLOID PEPTIDE, BETA-A4 25-35, MIMICS THE FUNCTION OF SUBSTANCE-P ON MODULATION OF NICOTINE-EVOKED SECRETION AND DESENSITIZATION IN CULTURED BOVINE ADRENAL CHROMAFFIN CELLS [J].

CHEUNG, NS ;

SMALL, DH ;

LIVETT, BG .

JOURNAL OF NEUROCHEMISTRY, 1993, 60 (03) :1163-1166