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Research ArticleBehavioral Pharmacology

Response of Neurotensin Basal Ganglia Systems during Extinction of Methamphetamine Self-Administration in Rat

Glen R. Hanson, Amanda J. Hoonakker, Christina M. Robson, Lisa M. McFadden, Paul S. Frankel and Mario E. Alburges
Journal of Pharmacology and Experimental Therapeutics August 2013, 346 (2) 173-181; DOI: https://doi.org/10.1124/jpet.113.205310
Glen R. Hanson
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah
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Amanda J. Hoonakker
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah
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Christina M. Robson
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah
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Lisa M. McFadden
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah
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Paul S. Frankel
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah
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Mario E. Alburges
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah
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Abstract

Because of persistent social problems caused by methamphetamine (METH), new therapeutic strategies need to be developed. Thus, we investigated the response of central nervous system neurotensin (NT) systems to METH self-administration (SA) and their interaction with basal ganglia dopamine (DA) pathways. Neurotensin is a peptide associated with inhibitory feedback pathways to nigrostriatal DA projections. We observed that NT levels decreased in rats during extinction of METH SA when lever pressing resulted in intravenous infusions of saline rather than METH. Thus, 6 h after the first session of extinction, NT levels were 53, 42, and 49% of corresponding controls in the anterior dorsal striatum, posterior dorsal striatum, and globus pallidus, respectively. NT levels were also significantly reduced in corresponding yoked rats in the anterior dorsal striatum (64% of control), but not the other structures examined. The reductions in NT levels in the anterior dorsal striatum particularly correlated with the lever pressing during the first session of extinction (r =s; 0.745). These, and previously reported findings, suggest that the extinction-related reductions in NT levels were mediated by activation of D2 receptors. Finally, administration of the neurotensin receptor 1 (NTR1) agonist [PD149163 [Lys(CH2NH)Lys-Pro,Trp-tert-Leu-Leu-Oet]; 0.25 or 0.5 mg/kg] diminished lever pressing during the first extinction session, whereas the NTR1 antagonist [SR48692 [2-[(1-(7-chloro-4-quinolinyl)-5-(2,6-imethoxyphenyl)pyrazol-3-yl)carbonylamino]tricyclo(3.3.1.1.(3.7))decan-2-carboxylic acid]; 0.3 mg/kg per administration] attenuated the reduction of lever pressing during the second to fourth days of extinction. In summary, these findings support the hypothesis that some of the endogenous basal ganglia NT systems contribute to the elimination of contingent behavior during the early stages of the METH SA extinction process.

Footnotes

    • Received April 2, 2013.
    • Accepted May 17, 2013.
  • This research was supported by the National Institutes of Health National Institute on Drug Abuse [Grants DA031883, DA000378, DA013367].

  • dx.doi.org/10.1124/jpet.113.205310.

  • Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 346 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 346, Issue 2
1 Aug 2013
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Research ArticleBehavioral Pharmacology

Neurotensin’s Role in METH Self-Administration Extinction

Glen R. Hanson, Amanda J. Hoonakker, Christina M. Robson, Lisa M. McFadden, Paul S. Frankel and Mario E. Alburges
Journal of Pharmacology and Experimental Therapeutics August 1, 2013, 346 (2) 173-181; DOI: https://doi.org/10.1124/jpet.113.205310

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Research ArticleBehavioral Pharmacology

Neurotensin’s Role in METH Self-Administration Extinction

Glen R. Hanson, Amanda J. Hoonakker, Christina M. Robson, Lisa M. McFadden, Paul S. Frankel and Mario E. Alburges
Journal of Pharmacology and Experimental Therapeutics August 1, 2013, 346 (2) 173-181; DOI: https://doi.org/10.1124/jpet.113.205310
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