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    Nicotinic acetylcholine receptors containing the alpha6 subunit contribute to ethanol activation of ventral tegmental area dopaminergic neurons

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    Authors
    Liu, Liwang
    Zhao-Shea, Rubing
    McIntosh, J. Michael
    Tapper, Andrew R.
    UMass Chan Affiliations
    Tapper Lab
    Brudnick Neuropsychiatric Research Institute
    Department of Psychiatry
    Document Type
    Journal Article
    Publication Date
    2013-10-15
    Keywords
    Animals
    Dopamine
    Dopaminergic Neurons
    Ethanol
    Mice
    Mice, Knockout
    Protein Subunits
    Receptors, Nicotinic
    Ventral Tegmental Area
    Chemical and Pharmacologic Phenomena
    Neuroscience and Neurobiology
    Pharmacology, Toxicology and Environmental Health
    Psychiatry
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    Link to Full Text
    http://dx.doi.org/10.1016/j.bcp.2013.06.015
    Abstract
    Nicotine and alcohol are often co-abused suggesting a common mechanism of action may underlie their reinforcing properties. Both drugs acutely increase activity of ventral tegmental area (VTA) dopaminergic (DAergic) neurons, a phenomenon associated with reward behavior. Recent evidence indicates that nicotinic acetylcholine receptors (nAChRs), ligand-gated cation channels activated by ACh and nicotine, may contribute to ethanol-mediated activation of VTA DAergic neurons although the nAChR subtype(s) involved has not been fully elucidated. Here we show that expression and activation of nAChRs containing the alpha6 subunit contribute to ethanol-induced activation of VTA DAergic neurons. In wild-type (WT) mouse midbrain sections that contain the VTA, ethanol (50 or 100 mM) significantly increased firing frequency of DAergic neurons. In contrast, ethanol did not significantly increase activity of VTA DAergic neurons in mice that do not express CHRNA6, the gene encoding the alpha6 nAChR subunit (alpha6 knock-out (KO) mice). Ethanol-induced activity in WT slices was also reduced by pre-application of the alpha6 subtype-selective nAChR antagonist, alpha-conotoxin MII[E11A]. When co-applied, ethanol potentiated the response to ACh in WT DAergic neurons; whereas co-application of ACh and ethanol failed to significantly increase activity of DAergic neurons in alpha6 KO slices. Finally, pre-application of alpha-conotoxin MII[E11A] in WT slices reduced ethanol potentiation of ACh responses. Together our data indicate that alpha6-subunit containing nAChRs may contribute to ethanol activation of VTA DAergic neurons. These receptors are predominantly expressed in DAergic neurons and known to be critical for nicotine reinforcement, providing a potential common therapeutic molecular target to reduce nicotine and alcohol co-abuse.
    Source

    Liu L, Zhao-Shea R, McIntosh JM, Tapper AR. Nicotinic acetylcholine receptors containing the α6 subunit contribute to ethanol activation of ventral tegmental area dopaminergic neurons. Biochem Pharmacol. 2013 Oct 15;86(8):1194-200. doi:10.1016/j.bcp.2013.06.015. Link to article on publisher's site

    DOI
    10.1016/j.bcp.2013.06.015
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/30138
    PubMed ID
    23811312
    Related Resources

    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1016/j.bcp.2013.06.015
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