Ethanol drinking-in-the-dark facilitates behavioral sensitization to ethanol in C57BL/6J, BALB/cByJ, but not in mu-opioid receptor deficient CXBK mice
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Otros documentos de la autoría: Tarragon Cros, Ernesto; Baliño, Pablo; González Aragón, Carlos Manuel; Pastor Medall, Raúl
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Título
Ethanol drinking-in-the-dark facilitates behavioral sensitization to ethanol in C57BL/6J, BALB/cByJ, but not in mu-opioid receptor deficient CXBK miceFecha de publicación
2012Editor
ElsevierISSN
0091-3057; 1873-5177Tipo de documento
info:eu-repo/semantics/articleVersión de la editorial
http://www.sciencedirect.com/science/article/pii/S0091305711003698Versión
info:eu-repo/semantics/publishedVersionPalabras clave / Materias
Resumen
Background: Neuroplasticity associated with drug-induced behavioral sensitization has been associated with
excessive drug pursuit and consumption characteristic of addiction. Repeated intraperitoneal (ip) injections
of ... [+]
Background: Neuroplasticity associated with drug-induced behavioral sensitization has been associated with
excessive drug pursuit and consumption characteristic of addiction. Repeated intraperitoneal (ip) injections
of ethanol (EtOH) can induce psychomotor sensitization in mice. In terms of its clinical relevance, however, it
is important to determine whether this phenomenon can also be produced by voluntary EtOH consumption.
Methods: The present investigation used a drinking-in-the-dark (DID) methodology to induce high levels of
EtOH drinking in mice; EtOH replaces water for 2 or 4 h, starting 3 h after the beginning of the dark cycle.
Animals followed a 3-week DID protocol prior to an evaluation of EtOH-induced locomotor activity (acute and
repeated EtOH). For the first week, animals had access to 20% EtOH. On weeks 2 and 3, different concentrations
of EtOH (10, 20 or 30%) were used. Three different inbred strains of mice were used: C57BL/6J (B6), BALB/cByJ
(BALB), and CXBK. The CXBK mouse line was used because of its reduced expression and functioning of brain
mu-opioid receptors, which have been suggested to participate in the development of EtOH-induced sensitization. B6 and BALB mice were used as controls.
Results: B6 and CXBK mice presented comparable levels of EtOH drinking (approx. 3 g/kg in 2 h), that were
higher than those showed by BALB. All animals, regardless of genotype, adjusted volume of EtOH intake to
obtain stable g/kg of EtOH across concentrations. Previous EtOH DID produced (B6) or potentiated (BALB)
sensitization to EtOH; this effect was not seen in CXBK. Western blot analysis showed a reduced number of
mu-opioid receptors in several brain regions of CXBK as compared to that of B6 and BALB mice.
Conclusions: In summary, here we show that the DID methodology can be used to trigger EtOH-induced
neuroplasticity supporting psychomotor sensitization, a process that might require participation of muopioid receptors. [-]
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Pharmacology, Biochemistry and Behavior 101 (2012)Derechos de acceso
© 2011 Elsevier Inc. All rights reserved.
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