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Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala.

Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala. Research Abstract Details 

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  • Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala. Abstract Text:

    yu zhaoYu Zhao,christopher v dayasChristopher V Dayas,harinder aujlaHarinder Aujla,marco a s baptistaMarco A S Baptista, martin-fardon Martin-Fardon,friedbert weissFriedbert Weiss,

    Major precipitating factors for relapse to drug use are stress and exposure to drug-related environmental stimuli. Group II (mGlu(2/3)) metabotropic glutamate receptors (mGluRs) are densely expressed within circuitries mediating the motivating effects of stress and drug cues and, therefore, may participate in regulating drug-seeking linked to both of these risk factors. Thus, we tested the hypothesis that pharmacological activation of group II mGluRs modifies both stress- and cue-induced ethanol-seeking, using reinstatement models of relapse. In parallel, brain c-fos expression was examined to identify neural substrates for the behavioral effects of group II mGluR activation. The selective mGlu(2/3) agonist LY379268 (1R,4R,5S,6R-2-oxa-4-aminobicyclo[3.1.0]hexane-4,6-dicarboxylate) (0.3, 1.0, and 3.0 mg/kg, s.c.) dose dependently blocked the recovery of extinguished ethanol-seeking induced by either footshock stress or ethanol-associated discriminative stimuli. These effects were accompanied by modulation of c-fos expression in the hippocampus, central nucleus of the amygdala, bed nucleus of the stria terminalis, and medial parvocellular paraventricular nucleus of the hypothalamus. The results implicate group II mGluRs as a shared neuropharmacological substrate for ethanol-seeking elicited by both drug cues and stress and identify group II mGluRs as promising treatment targets for relapse prevention.

    Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala. Publishing Authors By Initials

    y zhaoY Zhao,cv dayasCV Dayas,h aujlaH Aujla,ma baptistaMA Baptista,r martin-fardonR Martin-Fardon,f weissF Weiss,

    For similar synaptic transmission research abstracts see: synaptic transmission research

    PUBMED ID PMID:

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    Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of neuroscience : the official journal

    VOLUME: 26

    Page Numbers: 9967-74

    Journal Abbreviation: J. Neurosci.

    ISSN: 1529-2401

    DAY: 27

    MONTH: Sep

    YEAR: 2006

    Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8102140

    Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala. Keywords Mesh Terms:

    KEYWORDS: Synaptic Transmission

    MESH TERMS: drug effects

    Chemical & Substance for Abstract: Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala. Information

    Substance Name: Ethanol

    Registry Number: 64-17-5

    Grant and Affiliation Information for Activation of group II metabotropic glutamate receptors attenuates both stress and cue-induced ethanol-seeking and modulates c-fos expression in the hippocampus and amygdala.

    AFFILIATION: Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, California 92037, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAAA

    GRANT: AA10531

    ACRONYM: AA

    MEDLINETA: J Neurosci

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    ACCESSION NUMBER:

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