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Research ArticleNeuropharmacology

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β1 and β2 Adrenergic Receptors

Oliver Vranjkovic, Shona Hang, David A. Baker and John R. Mantsch
Journal of Pharmacology and Experimental Therapeutics August 2012, 342 (2) 541-551; DOI: https://doi.org/10.1124/jpet.112.193615
Oliver Vranjkovic
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Shona Hang
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David A. Baker
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John R. Mantsch
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Abstract

Stress can trigger the relapse of drug use in recovering cocaine addicts and reinstatement in rodent models through mechanisms that may involve norepinephrine release and β-adrenergic receptor activation. The present study examined the role of β-adrenergic receptor subtypes in the stressor-induced reinstatement of extinguished cocaine-induced (15 mg/kg i.p.) conditioned place preference in mice. Forced swim (6 min at 22°C) stress or activation of central noradrenergic neurotransmission by administration of the selective α2 adrenergic receptor antagonist 2-[(4,5-dihydro-1H-imidazol-2-yl)methyl]-2,3-dihydro-1-methyl-1H-isoindole (BRL-44,408) (10 mg/kg i.p.) induced reinstatement in wild-type, but not β- adrenergic receptor-deficient Adrb1/Adrb2 double-knockout, mice. In contrast, cocaine administration (15 mg/kg i.p.) resulted in reinstatement in both wild-type and β-adrenergic receptor knockout mice. Stress-induced reinstatement probably involved β2 adrenergic receptors. The β2 adrenergic receptor antagonist -(isopropylamino)-1-[(7-methyl-4-indanyl)oxy]butan-2-ol (ICI-118,551) (1 or 2 mg/kg i.p.) blocked reinstatement by forced swim or BRL-44,408, whereas administration of the nonselective β-adrenergic receptor agonist isoproterenol (2 or 4 mg/kg i.p.) or the β2 adrenergic receptor-selective agonist clenbuterol (2 or 4 mg/kg i.p.) induced reinstatement. Forced swim-induced, but not BRL-44,408-induced, reinstatement was also blocked by a high (20 mg/kg) but not low (10 mg/kg) dose of the β1 adrenergic receptor antagonist betaxolol, and isoproterenol-induced reinstatement was blocked by pretreatment with either ICI-118,551 or betaxolol, suggesting a potential cooperative role for β1 and β2 adrenergic receptors in stress-induced reinstatement. Overall, these findings suggest that targeting β-adrenergic receptors may represent a promising pharmacotherapeutic strategy for preventing drug relapse, particularly in cocaine addicts whose drug use is stress related.

Footnotes

  • This work was supported by the National Institutes of Health National Institute on Drug Abuse [Grants DA015758, DA017328].

  • Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.

    http://dx.doi.org/10.1124/jpet.112.193615.

  • ABBREVIATIONS:

    WT
    wild type
    KO
    knockout
    ANOVA
    analysis of variance
    BNST
    bed nucleus of the stria terminalis
    CRF
    corticotrophin-releasing factor
    VTA
    ventral tegmental area
    BRL-44,408
    2-[(4,5-dihydro-1H-imidazol-2-yl)methyl]-2,3-dihydro-1-methyl-1H-isoindole
    ICI-118,551
    -(isopropylamino)-1-[(7-methyl-4-indanyl)oxy]butan-2-ol.

  • Received February 23, 2012.
  • Accepted May 15, 2012.
  • Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 342 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 342, Issue 2
1 Aug 2012
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Research ArticleNeuropharmacology

β-Adrenergic Receptor Mediation of Stress-Induced Relapse

Oliver Vranjkovic, Shona Hang, David A. Baker and John R. Mantsch
Journal of Pharmacology and Experimental Therapeutics August 1, 2012, 342 (2) 541-551; DOI: https://doi.org/10.1124/jpet.112.193615

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Research ArticleNeuropharmacology

β-Adrenergic Receptor Mediation of Stress-Induced Relapse

Oliver Vranjkovic, Shona Hang, David A. Baker and John R. Mantsch
Journal of Pharmacology and Experimental Therapeutics August 1, 2012, 342 (2) 541-551; DOI: https://doi.org/10.1124/jpet.112.193615
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