Chronic nicotine modifies the effects of morphine on extracellular striatal dopamine and ventral tegmental GABA

Tanja Vihavainen, Toni Relander, Riikka Leiviskä, Mikko Airavaara, Raimo K Tuominen, Liisa Ahtee, Timo Petteri Piepponen

    Research output: Contribution to journalArticleScientificpeer-review

    Abstract

    Previously, we have shown that 7-week oral nicotine treatment enhances morphine-induced behaviors and dopaminergic activity in the mouse brain. In this study, we further characterized the nicotine-morphine interaction in the mesolimbic and nigrostriatal dopaminergic systems, as well as in the GABAergic control of these systems. In nicotine-pretreated mice, morphine-induced dopamine release in the caudate putamen and nucleus accumbens was significantly augmented, as measured by microdialysis. Chronic nicotine treatment did not change basal extracellular concentrations of dopamine and its metabolites in the caudate putamen and nucleus accumbens, nor did it affect the rate of dopamine synthesis, as assessed by 3-hydroxybenzylhydrazine dihydrochloride-induced DOPA accumulation. GABAergic control of dopaminergic activity was studied by measuring extracellular GABA in the presence of nipecotic acid, an inhibitor of GABA uptake. Acute (0.3 mg/kg or 0.5 mg/kg i.p.) and chronic nicotine, as well as morphine (15 mg/kg s.c.) in control mice decreased nipecotic acid-induced increase in extracellular GABA in the ventral tegmental area/substantia nigra (VTA/SN). In contrast, in nicotine-treated mice, morphine increased GABA levels in the presence of nipecotic acid. We did not find any alterations in GABA(B)-receptor function after chronic nicotine treatment. Thus, our data show that chronic nicotine treatment sensitizes dopaminergic systems to morphine and affects GABAergic systems in the VTA/SN.
    Original languageEnglish
    JournalJournal of Neurochemistry
    Volume107
    Issue number3
    Pages (from-to)844-854
    Number of pages11
    ISSN0022-3042
    DOIs
    Publication statusPublished - 2008
    MoE publication typeA1 Journal article-refereed

    Fields of Science

    • 317 Pharmacy

    Cite this

    @article{da42211801014ca6a66495666558a4b5,
    title = "Chronic nicotine modifies the effects of morphine on extracellular striatal dopamine and ventral tegmental GABA",
    abstract = "Previously, we have shown that 7-week oral nicotine treatment enhances morphine-induced behaviors and dopaminergic activity in the mouse brain. In this study, we further characterized the nicotine-morphine interaction in the mesolimbic and nigrostriatal dopaminergic systems, as well as in the GABAergic control of these systems. In nicotine-pretreated mice, morphine-induced dopamine release in the caudate putamen and nucleus accumbens was significantly augmented, as measured by microdialysis. Chronic nicotine treatment did not change basal extracellular concentrations of dopamine and its metabolites in the caudate putamen and nucleus accumbens, nor did it affect the rate of dopamine synthesis, as assessed by 3-hydroxybenzylhydrazine dihydrochloride-induced DOPA accumulation. GABAergic control of dopaminergic activity was studied by measuring extracellular GABA in the presence of nipecotic acid, an inhibitor of GABA uptake. Acute (0.3 mg/kg or 0.5 mg/kg i.p.) and chronic nicotine, as well as morphine (15 mg/kg s.c.) in control mice decreased nipecotic acid-induced increase in extracellular GABA in the ventral tegmental area/substantia nigra (VTA/SN). In contrast, in nicotine-treated mice, morphine increased GABA levels in the presence of nipecotic acid. We did not find any alterations in GABA(B)-receptor function after chronic nicotine treatment. Thus, our data show that chronic nicotine treatment sensitizes dopaminergic systems to morphine and affects GABAergic systems in the VTA/SN.",
    keywords = "317 Pharmacy",
    author = "Tanja Vihavainen and Toni Relander and Riikka Leivisk{\"a} and Mikko Airavaara and Tuominen, {Raimo K} and Liisa Ahtee and Piepponen, {Timo Petteri}",
    year = "2008",
    doi = "10.1111/j.1471-4159.2008.05676.x",
    language = "English",
    volume = "107",
    pages = "844--854",
    journal = "Journal of Neurochemistry",
    issn = "0022-3042",
    publisher = "LIPPINCOTT-RAVEN PUBL",
    number = "3",

    }

    Chronic nicotine modifies the effects of morphine on extracellular striatal dopamine and ventral tegmental GABA. / Vihavainen, Tanja; Relander, Toni; Leiviskä, Riikka; Airavaara, Mikko; Tuominen, Raimo K; Ahtee, Liisa; Piepponen, Timo Petteri.

    In: Journal of Neurochemistry, Vol. 107, No. 3, 2008, p. 844-854.

    Research output: Contribution to journalArticleScientificpeer-review

    TY - JOUR

    T1 - Chronic nicotine modifies the effects of morphine on extracellular striatal dopamine and ventral tegmental GABA

    AU - Vihavainen, Tanja

    AU - Relander, Toni

    AU - Leiviskä, Riikka

    AU - Airavaara, Mikko

    AU - Tuominen, Raimo K

    AU - Ahtee, Liisa

    AU - Piepponen, Timo Petteri

    PY - 2008

    Y1 - 2008

    N2 - Previously, we have shown that 7-week oral nicotine treatment enhances morphine-induced behaviors and dopaminergic activity in the mouse brain. In this study, we further characterized the nicotine-morphine interaction in the mesolimbic and nigrostriatal dopaminergic systems, as well as in the GABAergic control of these systems. In nicotine-pretreated mice, morphine-induced dopamine release in the caudate putamen and nucleus accumbens was significantly augmented, as measured by microdialysis. Chronic nicotine treatment did not change basal extracellular concentrations of dopamine and its metabolites in the caudate putamen and nucleus accumbens, nor did it affect the rate of dopamine synthesis, as assessed by 3-hydroxybenzylhydrazine dihydrochloride-induced DOPA accumulation. GABAergic control of dopaminergic activity was studied by measuring extracellular GABA in the presence of nipecotic acid, an inhibitor of GABA uptake. Acute (0.3 mg/kg or 0.5 mg/kg i.p.) and chronic nicotine, as well as morphine (15 mg/kg s.c.) in control mice decreased nipecotic acid-induced increase in extracellular GABA in the ventral tegmental area/substantia nigra (VTA/SN). In contrast, in nicotine-treated mice, morphine increased GABA levels in the presence of nipecotic acid. We did not find any alterations in GABA(B)-receptor function after chronic nicotine treatment. Thus, our data show that chronic nicotine treatment sensitizes dopaminergic systems to morphine and affects GABAergic systems in the VTA/SN.

    AB - Previously, we have shown that 7-week oral nicotine treatment enhances morphine-induced behaviors and dopaminergic activity in the mouse brain. In this study, we further characterized the nicotine-morphine interaction in the mesolimbic and nigrostriatal dopaminergic systems, as well as in the GABAergic control of these systems. In nicotine-pretreated mice, morphine-induced dopamine release in the caudate putamen and nucleus accumbens was significantly augmented, as measured by microdialysis. Chronic nicotine treatment did not change basal extracellular concentrations of dopamine and its metabolites in the caudate putamen and nucleus accumbens, nor did it affect the rate of dopamine synthesis, as assessed by 3-hydroxybenzylhydrazine dihydrochloride-induced DOPA accumulation. GABAergic control of dopaminergic activity was studied by measuring extracellular GABA in the presence of nipecotic acid, an inhibitor of GABA uptake. Acute (0.3 mg/kg or 0.5 mg/kg i.p.) and chronic nicotine, as well as morphine (15 mg/kg s.c.) in control mice decreased nipecotic acid-induced increase in extracellular GABA in the ventral tegmental area/substantia nigra (VTA/SN). In contrast, in nicotine-treated mice, morphine increased GABA levels in the presence of nipecotic acid. We did not find any alterations in GABA(B)-receptor function after chronic nicotine treatment. Thus, our data show that chronic nicotine treatment sensitizes dopaminergic systems to morphine and affects GABAergic systems in the VTA/SN.

    KW - 317 Pharmacy

    U2 - 10.1111/j.1471-4159.2008.05676.x

    DO - 10.1111/j.1471-4159.2008.05676.x

    M3 - Article

    VL - 107

    SP - 844

    EP - 854

    JO - Journal of Neurochemistry

    JF - Journal of Neurochemistry

    SN - 0022-3042

    IS - 3

    ER -