Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Neuronal-glial interactions mediated by interleukin-1 enhance neuronal acetylcholinesterase activity and mRNA expression
Autore:
Li, YK; Liu, L; Kang, JS; Sheng, JG; Barger, SW; Mrak, RE; Griffin, WST;
Indirizzi:
Univ Arkansas Med Sci, Donald W Reynolds Dept Geriatr, Little Rock, AR 72205 USA Univ Arkansas Med Sci Little Rock AR USA 72205 Little Rock, AR 72205 USA Univ Arkansas Med Sci, Dept Anat, Little Rock, AR 72205 USA Univ Arkansas Med Sci Little Rock AR USA 72205 Little Rock, AR 72205 USA Univ Arkansas Med Sci, Dept Pathol, Little Rock, AR 72205 USA Univ Arkansas Med Sci Little Rock AR USA 72205 Little Rock, AR 72205 USA Univ Arkansas Med Sci, Dept Med, Little Rock, AR 72205 USA Univ Arkansas Med Sci Little Rock AR USA 72205 Little Rock, AR 72205 USA Univ Arkansas Med Sci, Dept Psychiat, Little Rock, AR 72205 USA Univ Arkansas Med Sci Little Rock AR USA 72205 Little Rock, AR 72205 USA McClellan Mem Vet Affairs Med Ctr, Pathol Serv, Little Rock, AR 72205 USA McClellan Mem Vet Affairs Med Ctr Little Rock AR USA 72205 , AR 72205 USA McClellan Mem Vet Affairs Med Ctr, Mental Illness Res Educ & Clin Ctr, Little Rock, AR 72205 USA McClellan Mem Vet Affairs Med Ctr Little Rock AR USA 72205 , AR 72205 USA McClellan Mem Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Little Rock, AR 72205 USA McClellan Mem Vet Affairs Med Ctr Little Rock AR USA 72205, AR 72205 USA Norman Bethune Univ Med Sci, Dept Pathophysiol, Changchun 130021, Peoples R China Norman Bethune Univ Med Sci Changchun Peoples R China 130021 les R China
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 1, volume: 20, anno: 2000,
pagine: 149 - 155
SICI:
0270-6474(20000101)20:1<149:NIMBIE>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; LONG-TERM POTENTIATION; ALZHEIMERS-DISEASE; MESSENGER-RNA; MOLECULAR-FORMS; SENILE PLAQUES; SELECTIVE LOSS; RAT-BRAIN; CELL-LINE; CHOLINESTERASES;
Keywords:
acetylcholinesterase; Alzheimer's disease; beta-amyloid precursor protein; choline acetyltransferase; cholinergic systems; interleukin-1; neuronal cultures; neuronal stress; PC12 cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Griffin, WST Res Serv 151LR, 4300 W 7th St, Little Rock, AR 72205 USA Res Serv 151LR 4300 W 7th St Little Rock AR USA 72205 205 USA
Citazione:
Y.K. Li et al., "Neuronal-glial interactions mediated by interleukin-1 enhance neuronal acetylcholinesterase activity and mRNA expression", J NEUROSC, 20(1), 2000, pp. 149-155

Abstract

Cholinergic dysfunction in Alzheimer's disease has been attributed to stress-induced increases in acetylcholinesterase (AChE) activity. Interleukin-1(IL-1) is overexpressed in Alzheimer's disease, and stress-related changesin long-term potentiation, an ACh-related cerebral function, are triggeredby interleukin-1. Microglial cultures (N9) synthesized and released IL-1 in response to conditioned media obtained from glutamate-treated primary neuron cultures or PC12 cells. This conditioned media contained elevated levels of secreted beta-amyloid precursor protein (sAPP). Naive PC12 cells cocultured with stimulated N9 cultures showed increased AChE activity and mRNA expression. These effects on AChE expression and activity could be blocked by either preincubating the glutamate-treated PC12 supernatants with anti-sAPP antibodies or preincubating naive PC12 cells with IL-1 receptor antagonist. These findings were confirmed in vivo; IL-1-containing pellets implanted into rat cortex also increased AChE mRNA levels. Neuronal stress in Alzheimer's disease may induce increases in AChE expression and activity througha molecular cascade that is mediated by sAPP-induced microglial activationand consequent overexpression of IL-1.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 06:04:05