Resistance to ethanol sensitization is associated with increased NMDA receptor binding in specific brain areas

Resistance to ethanol sensitization is associated with increased NMDA receptor binding in specific brain areas

Autor Quadros, IMH Google Scholar
Hipolide, D. C. Google Scholar
Frussa, R. Google Scholar
De Lucca, E. M. Google Scholar
Nobrega, J. N. Google Scholar
Souza-Formigoni, MLO Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Ctr Addict & Mental Hlth
Resumo Co-administration of N-methyl- D-aspartate (NMDA) receptor antagonists is known to block the development of behavioral sensitization to ethanol and other psycho stimulants. Since ethanol sensitization in mice does not occur uniformly in all treated animals, the present study examined the possibility that NMDA receptor binding would be selectively altered in mice susceptible to ethanol sensitization. Mice received 2.4 g/kg ethanol or saline i.p. daily for 21 days and were sacrificed 24 It later. No differences in [H-3]dizoeilpine ([H-3]( -)MK-801) binding were found between sensitized and vehicle-treated mice in any of the brain regions analyzed. However, ethanol-treated mice that did not develop sensitization showed significantly higher binding in the nucleus accumbens core (+ 32% and 40% compared to controls and ethanol-sensitized mice, respectively; P<0.04) and the prefrontal cortex (+15% and +22%; P<0.02). in a separate experiment, sensitization resistant mice challenged with 0.25 mg/kg (+)MK 801 showed significantly less motor activation than saline-treated or ethanol-sensitized mice. These results point to a clear association between elevated NMDA receptor binding in specific brain regions and resistance to ethanol sensitization. (C) 2002 Elsevier Science B.V. All rights reserved.
Palavra-chave [H-3](+)MK-801
nucleus accumbens
cortex, prefrontal
Idioma Inglês
Data de publicação 2002-05-03
Publicado em European Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 442, n. 1-2, p. 55-61, 2002.
ISSN 0014-2999 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 55-61
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000176080900007
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