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Titolo:
Change of cholinergic transmission and memory deficiency induced by injection of beta-amyloid protein into NBM of rats
Autore:
Ma, XF; Ye, WL; Mei, ZT;
Indirizzi:
Chinese Acad Sci, Shanghai Inst Physiol, Shanghai 200031, Peoples R China Chinese Acad Sci Shanghai Peoples R China 200031 200031, Peoples R China
Titolo Testata:
SCIENCE IN CHINA SERIES C-LIFE SCIENCES
fascicolo: 4, volume: 44, anno: 2001,
pagine: 435 - 442
SICI:
1006-9305(200108)44:4<435:COCTAM>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACETYLCHOLINE-RELEASE; ALZHEIMERS-DISEASE; BEHAVIOR; CORTEX;
Keywords:
beta-amyloid protein; nucleus basalis magnocellularis; cholinergic transmission in frontal cortex; microdialysis sampling; working memory; rats;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Mei, ZT Chinese Acad Sci, Shanghai Inst Physiol, Shanghai 200031, Peoples R China Chinese Acad Sci Shanghai Peoples R China 200031 Peoples R China
Citazione:
X.F. Ma et al., "Change of cholinergic transmission and memory deficiency induced by injection of beta-amyloid protein into NBM of rats", SCI CHINA C, 44(4), 2001, pp. 435-442

Abstract

The change of cholinergic transmission of beta -amyloid protein (beta -AP)treated rats was studied by intracerebral microdialysis sampling combined with HPLC analysis. beta -AP(1-40) was injected into nucleus basalis magnocellularis (NBM). Passive avoidance response test (step-down test) and delayed alternation task were used for memory testing. The impairment of memory after injection of beta -AP(1-40) into NBM exhibited mainly the deficiency of short-term working memory. One week after injection of beta -AP(1-40) the release of acetylcholine (ACh) from frontal cortex of freely-moving rats decreased significantly, and the response of cholinergic nerve ending to the action of high [K+] solution was rather weak. In control animals the percentage of increase of ACh-release during behavioral performance was 57%, while in beta -AP(1-40)-treated rats it was 34%. The temporary increase of the ACh-release of the rat put into a new place was also significantly diminished in beta -AP(1-40)-treated rats. The results show that the injection ofbeta -AP(1-40) into NBM impairs the cholinergic transmission in frontal cortex, and the impairment of cholinergic transmission may be the main cause of the deficit of working memory.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 22:42:30