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Dependence-induced ethanol drinking and GABA neurotransmission are altered in Alk deficient mice.

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Title: Dependence-induced ethanol drinking and GABA neurotransmission are altered in Alk deficient mice.
Author(s): Schweitzer, P.; Cates-Gatto, C.; Varodayan, F.P.; Nadav, T.; Roberto, M.; Lasek, A.W.; Roberts, A.J.
Subject(s): Addiction ALK Amygdala Chronic intermittent ethanol GABA Synaptic
Abstract: Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that is expressed in the brain and implicated in alcohol abuse in humans and behavioral responses to ethanol in mice. Previous studies have shown an association of human ALK with acute responses to alcohol and alcohol dependence. In addition, Alk knockout (Alk -/-) mice consume more ethanol in a binge-drinking test and show increased sensitivity to ethanol sedation. However, the function of ALK in excessive drinking following the establishment of ethanol dependence has not been examined. In this study, we tested Alk -/- mice for dependence-induced drinking using the chronic intermittent ethanol-two bottle choice drinking (CIE-2BC) protocol. We found that Alk -/- mice initially consume more ethanol prior to CIE exposure, but do not escalate ethanol consumption after exposure, suggesting that ALK may promote the escalation of drinking after ethanol dependence. To determine the mechanism(s) responsible for this behavioral phenotype we used an electrophysiological approach to examine GABA neurotransmission in the central nucleus of the amygdala (CeA), a brain region that regulates alcohol consumption and shows increased GABA signaling after chronic ethanol exposure. GABA transmission in ethanol-naïve Alk -/- mice was enhanced at baseline and potentiated in response to acute ethanol application when compared to wild-type (Alk +/+) mice. Moreover, basal GABA transmission was not elevated by CIE exposure in Alk -/- mice as it was in Alk +/+ mice. These data suggest that ALK plays a role in dependence-induced drinking and the regulation of presynaptic GABA release in the CeA.
Issue Date: 2016-03
Publisher: Elsevier
Citation Info: Schweitzer, P., Cates-Gatto, C., Varodayan, F. P., Nadav, T., Roberto, M., Lasek, A. W. and Roberts, A. J. Dependence-induced ethanol drinking and GABA neurotransmission are altered in Alk deficient mice. Neuropharmacology. 2016. 107: 1-8. DOI: 10.1016/j.neuropharm.2016.03.003
Type: Article
Description: NOTICE: This is the author’s version of a work that was accepted for publication in Neuropharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Neuropharmacology 2016. 107: 1-8 DOI: 10.1016/j.neuropharm.2016.03.003.
URI: http://hdl.handle.net/10027/20705
ISSN: 0028-3908
Sponsor: National Institute on Alcohol Abuse and Alcoholism (Integrative Neuroscience Initiative on Alcoholism, AA020912 and AA016654 to A.W.L., AA020893 to A.J.R., AA013498 to M.R., and AA013517 to P.S.). This is manuscript #29266 from The Scripps Research Institute.
Date Available in INDIGO: 2017-12-09
 

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