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Stress potentiation of morphine-induced dopamine efflux in the nucleus accumbens shell is dependent upon stressor uncontrollability and is mediated by the dorsal raphe nucleus.
Neuroscience. 2004; 126(3):705-15.N

Abstract

A single session of uncontrollable (inescapable tailshock, IS), but not controllable (escapable tailshock, ES), stress is known to selectively potentiate subsequent morphine-conditioned place preference in a dorsal raphe nucleus (DRN) serotonin (5-HT) dependent manner. Here, in vivo microdialysis is used to test the hypothesis that prior IS, but not ES, will potentiate morphine-induced dopamine (DA) efflux in the nucleus accumbens (NAc) shell and that this will occur by a pathway involving DRN 5-HT neurons. Male Sprague-Dawley rats were exposed to yoked IS, ES, or no stress. Twenty-four hours later, morphine (3 mg/kg s.c.) or saline was administered during microdialysis. As predicted, prior IS selectively potentiated morphine-induced DA, but not 5-HT, efflux in the NAc. This potentiation was due to morphine's action in the DRN because it was blocked by intra-DRN microinjection of the opioid antagonist naltrexone (10 microg). IS potentiation of morphine-induced DA efflux in the NAc was also dependent upon activation of 5-HT neurons in the DRN because it was blocked by intra-DRN microinjection of the 5-HT1A autoreceptor agonist 8-hydroxy-2-di-n-(propylamino)-tetralin (1 microg). No effect of IS was found on morphine-induced 5-HT or DA efflux in the ventral tegmental area. These results suggest a neural substrate for stress potentiation of morphine reward involving 5-HT neurotransmission in the DRN.

Authors+Show Affiliations

Department of Psychology and Center for Neuroscience, Campus Box 345, University of Colorado, Boulder, CO 80309-0345, USA. sondra.bland@colorado.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15183519

Citation

Bland, S T., et al. "Stress Potentiation of Morphine-induced Dopamine Efflux in the Nucleus Accumbens Shell Is Dependent Upon Stressor Uncontrollability and Is Mediated By the Dorsal Raphe Nucleus." Neuroscience, vol. 126, no. 3, 2004, pp. 705-15.
Bland ST, Twining C, Schmid MJ, et al. Stress potentiation of morphine-induced dopamine efflux in the nucleus accumbens shell is dependent upon stressor uncontrollability and is mediated by the dorsal raphe nucleus. Neuroscience. 2004;126(3):705-15.
Bland, S. T., Twining, C., Schmid, M. J., Der-Avakian, A., Watkins, L. R., & Maier, S. F. (2004). Stress potentiation of morphine-induced dopamine efflux in the nucleus accumbens shell is dependent upon stressor uncontrollability and is mediated by the dorsal raphe nucleus. Neuroscience, 126(3), 705-15.
Bland ST, et al. Stress Potentiation of Morphine-induced Dopamine Efflux in the Nucleus Accumbens Shell Is Dependent Upon Stressor Uncontrollability and Is Mediated By the Dorsal Raphe Nucleus. Neuroscience. 2004;126(3):705-15. PubMed PMID: 15183519.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Stress potentiation of morphine-induced dopamine efflux in the nucleus accumbens shell is dependent upon stressor uncontrollability and is mediated by the dorsal raphe nucleus. AU - Bland,S T, AU - Twining,C, AU - Schmid,M J, AU - Der-Avakian,A, AU - Watkins,L R, AU - Maier,S F, PY - 2004/04/08/accepted PY - 2004/6/9/pubmed PY - 2004/9/15/medline PY - 2004/6/9/entrez SP - 705 EP - 15 JF - Neuroscience JO - Neuroscience VL - 126 IS - 3 N2 - A single session of uncontrollable (inescapable tailshock, IS), but not controllable (escapable tailshock, ES), stress is known to selectively potentiate subsequent morphine-conditioned place preference in a dorsal raphe nucleus (DRN) serotonin (5-HT) dependent manner. Here, in vivo microdialysis is used to test the hypothesis that prior IS, but not ES, will potentiate morphine-induced dopamine (DA) efflux in the nucleus accumbens (NAc) shell and that this will occur by a pathway involving DRN 5-HT neurons. Male Sprague-Dawley rats were exposed to yoked IS, ES, or no stress. Twenty-four hours later, morphine (3 mg/kg s.c.) or saline was administered during microdialysis. As predicted, prior IS selectively potentiated morphine-induced DA, but not 5-HT, efflux in the NAc. This potentiation was due to morphine's action in the DRN because it was blocked by intra-DRN microinjection of the opioid antagonist naltrexone (10 microg). IS potentiation of morphine-induced DA efflux in the NAc was also dependent upon activation of 5-HT neurons in the DRN because it was blocked by intra-DRN microinjection of the 5-HT1A autoreceptor agonist 8-hydroxy-2-di-n-(propylamino)-tetralin (1 microg). No effect of IS was found on morphine-induced 5-HT or DA efflux in the ventral tegmental area. These results suggest a neural substrate for stress potentiation of morphine reward involving 5-HT neurotransmission in the DRN. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/15183519/Stress_potentiation_of_morphine_induced_dopamine_efflux_in_the_nucleus_accumbens_shell_is_dependent_upon_stressor_uncontrollability_and_is_mediated_by_the_dorsal_raphe_nucleus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306452204002738 DB - PRIME DP - Unbound Medicine ER -