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Titolo:
Effect of nicotine on cerebellar granule neuron development
Autore:
Opanashuk, LA; Pauly, JR; Hauser, KF;
Indirizzi:
Univ Kentucky, Coll Med, Dept Anat & Neurobiol, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 & Neurobiol, Lexington, KY 40536 USA Univ Kentucky, Coll Pharm, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 Coll Pharm, Lexington, KY 40536 USA Univ Kentucky, Coll Med, Lucille P Markey Canc Ctr, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 ey Canc Ctr, Lexington, KY 40536 USA
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 1, volume: 13, anno: 2001,
pagine: 48 - 56
SICI:
0953-816X(200101)13:1<48:EONOCG>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBROBLAST GROWTH-FACTOR; RECEPTOR-BINDING SITES; SUBUNIT MESSENGER-RNAS; SMOOTH-MUSCLE CELLS; LUNG-CANCER CELLS; RAT-BRAIN REGIONS; ACETYLCHOLINE-RECEPTORS; POSTNATAL-DEVELOPMENT; CHOLINERGIC SYSTEM; DEPENDENT CARCINOGENESIS;
Keywords:
alpha 3 nicotinic receptor subunits; cerebellar development; neuroblast proliferation; neurogenesis; nicotinic receptors; programmed cell death;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
75
Recensione:
Indirizzi per estratti:
Indirizzo: Hauser, KF Univ Kentucky, Coll Med, Dept Anat & Neurobiol, 800 Rose St, Lexington, KY40536 USA Univ Kentucky 800 Rose St Lexington KY USA 40536 n, KY40536 USA
Citazione:
L.A. Opanashuk et al., "Effect of nicotine on cerebellar granule neuron development", EUR J NEURO, 13(1), 2001, pp. 48-56

Abstract

To assess the role of nicotinic cholinergic receptors (nAChR) on neuronal maturation, nAChR expression and the direct effects of nAChR activation were examined in cerebellar external granular layer (EGL) precursors isolated in vitro. Treatment of EGL neuroblasts with nicotine elicited a concentration-dependent increase in DNA content and synthesis, implying an increase incell numbers. Pretreatment of cultures with the nAChR antagonist dihydro-beta -erythroidine (DHBE) attenuated nicotine-induced changes in DNA abundance and synthesis. Furthermore, chronic nicotine treatment for 4-7 days promoted EGL cell survival. Epibatidine but not cytisine stimulated granule neuroblast DNA synthesis and survival. Survival effects mediated by nicotine and epibatidine were attenuated by pretreating cultures with DHBE. Immunocytochemical analysis revealed that EGL neurons possessed alpha3, but not alpha4, nAChR immunoreactivity. Quantitative autoradiography was used to determine which nAChRs are present during the period of granule cell neurogenesisin vivo. On postnatal day 5, the EGL was intensely labelled by [H-3]-epibatidine but virtually devoid of [H-3]-A85380 binding, suggesting that a highconcentration of alpha3 AChRs is present in granule neuroblasts. The pharmacology of [H-3]-epibatidine displacement from EGL neurons also suggested an interaction with the alpha3-nAChR subunits. Together these data provide novel evidence that the activation of nAChRs directly affect the developmentof primary cerebellar neuroblasts and further suggest that the effects aremediated through the alpha3-nAChR subtype.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 21:00:34