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| Research article summary (published 30 Mar 2009): |
Renewal and spontaneous recovery, but not latent inhibition, are mediated by gamma-aminobutyric acid in appetitive conditioning.
Full Abstract
Previous research has reported a role for the neurotransmitter gamma-aminobutyric acid (GABA) in the extinction and renewal of conditioned fear. Here, the authors examine whether GABA is involved in the acquisition, extinction, renewal, spontaneous recovery, and latent inhibition of appetitive conditioning. Using Long-Evans rats, systemic injection of the GABA A receptor inverse agonist FG 7142 was shown to eliminate ABA renewal (Experiment 1) and spontaneous recovery (Experiment 4) of appetitive responding by selectively reducing the recovery of extinguished magazine approach. Furthermore, treatment with FG 7142 had no effects on acquisition or single-session extinction (Experiment 3) or on the context-specific expression of latent inhibition (Experiment 2). These data suggest that ABA renewal and spontaneous recovery, but not latent inhibition or responding during acquisition and an initial extinction session, are mediated by GABAergic mechanisms in appetitive Pavlovian conditioning. They provide support for the view that renewal and spontaneous recovery share a common psychological mechanism. Copyright (c) 2009 APA, all rights reserved.
Author information
Author/s: Delamater, Andrew R (AR); Campese, Vincent (V); Westbrook, R Frederick (RF);
Affiliation: Department of Psychology, Brooklyn College-The City University of New York, Brooklyn, NY 11210, USA. andrewd(-atsign-)brooklyn.cuny.edu
Grants: MH65947-3 (Agency:NIMH NIH HHS)
Journal and publication information
Publication Type: Journal Article; Research Support, N.I.H., Extramural
Journal: Journal of experimental psychology. Animal behavior processes (J Exp Psychol Anim Behav Process), published in United States. (Language: eng)
Reference: 2009-Apr; vol 35 (issue 2) : pp 224-37
Dates: Created 2009/04/14; Completed 2009/06/25;
PMID: 19364231, status: MEDLINE (last retrieval date: 6/25/2009, IMS Date: 25 Jun 2009 00:00:00)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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