No evidence of a role of the β4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors

Helen M. Kamens, Constanza Silva, Riley McCarthy, Ryan J. Cox, Marissa A. Ehringer

    Research output: Contribution to journalArticle

    4 Citations (Scopus)

    Abstract

    Background: Nicotinic acetylcholine receptors have gained attention in the last several years as mediators of alcohol-related behaviors. The genes that code for the α5, α3, and β4 subunits (Chrna5, Chrna3, and Chrnb4, respectively) map adjacent to each other on human chromosome 15/mouse chromosome 9. Genetic variants in this region have been associated with alcohol phenotypes and mice that overexpress these three subunits have reduced ethanol intake. In the present experiments, we examined the role of the Chrnb4 gene in three ethanol behaviors: consumption, ataxia, and sedation. Wildtype, heterozygous, and knockout mice were tested for ethanol consumption with a 2-bottle choice procedure and the drinking-in-the-dark paradigm. Ethanol-induced ataxia was measured with the balance beam and dowel test. Finally, the sedative effects of ethanol were measured with the loss of righting reflex paradigm. Results: We observed no significant genotypic effects on any of the ethanol behaviors examined, suggesting that the β4 subunit is not involved in mediating these responses. Conclusions: While we found no evidence for the involvement of the β4 subunit in ethanol responses, it is possible that this subunit modulates other behaviors not tested and further work should address this before completely ruling out its involvement.

    Original languageEnglish (US)
    Article number151
    JournalBMC Research Notes
    Volume10
    Issue number1
    DOIs
    StatePublished - Apr 5 2017

    Fingerprint

    Nicotinic Receptors
    Ethanol
    Alcohols
    Ataxia
    Chromosomes
    Genes
    Righting Reflex
    Chromosomes, Human, Pair 15
    Chromosomes, Human, Pair 9
    Bottles
    Human Chromosomes
    Hypnotics and Sedatives
    Knockout Mice
    Drinking
    Phenotype

    All Science Journal Classification (ASJC) codes

    • Biochemistry, Genetics and Molecular Biology(all)

    Cite this

    Kamens, Helen M. ; Silva, Constanza ; McCarthy, Riley ; Cox, Ryan J. ; Ehringer, Marissa A. / No evidence of a role of the β4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors. In: BMC Research Notes. 2017 ; Vol. 10, No. 1.
    @article{fd320882f163481fbe07e230c234a849,
    title = "No evidence of a role of the β4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors",
    abstract = "Background: Nicotinic acetylcholine receptors have gained attention in the last several years as mediators of alcohol-related behaviors. The genes that code for the α5, α3, and β4 subunits (Chrna5, Chrna3, and Chrnb4, respectively) map adjacent to each other on human chromosome 15/mouse chromosome 9. Genetic variants in this region have been associated with alcohol phenotypes and mice that overexpress these three subunits have reduced ethanol intake. In the present experiments, we examined the role of the Chrnb4 gene in three ethanol behaviors: consumption, ataxia, and sedation. Wildtype, heterozygous, and knockout mice were tested for ethanol consumption with a 2-bottle choice procedure and the drinking-in-the-dark paradigm. Ethanol-induced ataxia was measured with the balance beam and dowel test. Finally, the sedative effects of ethanol were measured with the loss of righting reflex paradigm. Results: We observed no significant genotypic effects on any of the ethanol behaviors examined, suggesting that the β4 subunit is not involved in mediating these responses. Conclusions: While we found no evidence for the involvement of the β4 subunit in ethanol responses, it is possible that this subunit modulates other behaviors not tested and further work should address this before completely ruling out its involvement.",
    author = "Kamens, {Helen M.} and Constanza Silva and Riley McCarthy and Cox, {Ryan J.} and Ehringer, {Marissa A.}",
    year = "2017",
    month = "4",
    day = "5",
    doi = "10.1186/s13104-017-2470-7",
    language = "English (US)",
    volume = "10",
    journal = "BMC Research Notes",
    issn = "1756-0500",
    publisher = "BioMed Central",
    number = "1",

    }

    No evidence of a role of the β4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors. / Kamens, Helen M.; Silva, Constanza; McCarthy, Riley; Cox, Ryan J.; Ehringer, Marissa A.

    In: BMC Research Notes, Vol. 10, No. 1, 151, 05.04.2017.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - No evidence of a role of the β4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors

    AU - Kamens, Helen M.

    AU - Silva, Constanza

    AU - McCarthy, Riley

    AU - Cox, Ryan J.

    AU - Ehringer, Marissa A.

    PY - 2017/4/5

    Y1 - 2017/4/5

    N2 - Background: Nicotinic acetylcholine receptors have gained attention in the last several years as mediators of alcohol-related behaviors. The genes that code for the α5, α3, and β4 subunits (Chrna5, Chrna3, and Chrnb4, respectively) map adjacent to each other on human chromosome 15/mouse chromosome 9. Genetic variants in this region have been associated with alcohol phenotypes and mice that overexpress these three subunits have reduced ethanol intake. In the present experiments, we examined the role of the Chrnb4 gene in three ethanol behaviors: consumption, ataxia, and sedation. Wildtype, heterozygous, and knockout mice were tested for ethanol consumption with a 2-bottle choice procedure and the drinking-in-the-dark paradigm. Ethanol-induced ataxia was measured with the balance beam and dowel test. Finally, the sedative effects of ethanol were measured with the loss of righting reflex paradigm. Results: We observed no significant genotypic effects on any of the ethanol behaviors examined, suggesting that the β4 subunit is not involved in mediating these responses. Conclusions: While we found no evidence for the involvement of the β4 subunit in ethanol responses, it is possible that this subunit modulates other behaviors not tested and further work should address this before completely ruling out its involvement.

    AB - Background: Nicotinic acetylcholine receptors have gained attention in the last several years as mediators of alcohol-related behaviors. The genes that code for the α5, α3, and β4 subunits (Chrna5, Chrna3, and Chrnb4, respectively) map adjacent to each other on human chromosome 15/mouse chromosome 9. Genetic variants in this region have been associated with alcohol phenotypes and mice that overexpress these three subunits have reduced ethanol intake. In the present experiments, we examined the role of the Chrnb4 gene in three ethanol behaviors: consumption, ataxia, and sedation. Wildtype, heterozygous, and knockout mice were tested for ethanol consumption with a 2-bottle choice procedure and the drinking-in-the-dark paradigm. Ethanol-induced ataxia was measured with the balance beam and dowel test. Finally, the sedative effects of ethanol were measured with the loss of righting reflex paradigm. Results: We observed no significant genotypic effects on any of the ethanol behaviors examined, suggesting that the β4 subunit is not involved in mediating these responses. Conclusions: While we found no evidence for the involvement of the β4 subunit in ethanol responses, it is possible that this subunit modulates other behaviors not tested and further work should address this before completely ruling out its involvement.

    UR - http://www.scopus.com/inward/record.url?scp=85016972446&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=85016972446&partnerID=8YFLogxK

    U2 - 10.1186/s13104-017-2470-7

    DO - 10.1186/s13104-017-2470-7

    M3 - Article

    C2 - 28381286

    AN - SCOPUS:85016972446

    VL - 10

    JO - BMC Research Notes

    JF - BMC Research Notes

    SN - 1756-0500

    IS - 1

    M1 - 151

    ER -