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No evidence of a role of the β 4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors

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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.

Electronic supplementary material: The online version of this article (doi:10.1186/s13104-017-2470-7) contains supplementary material, which is available to authorized users.

No MeSH data available.


Deletion of the Chrnb4 gene does not modulate binge-like ethanol consumption. Data (mean ± SEM) represent 4 h ethanol consumption (a), BEC after 4 h ethanol intake (b), and 4 h sucrose consumption (c). Female WT = 6, HET = 7, KO = 6; Male WT = 5, HET = 6, KO = 4
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Fig3: Deletion of the Chrnb4 gene does not modulate binge-like ethanol consumption. Data (mean ± SEM) represent 4 h ethanol consumption (a), BEC after 4 h ethanol intake (b), and 4 h sucrose consumption (c). Female WT = 6, HET = 7, KO = 6; Male WT = 5, HET = 6, KO = 4

Mentions: Deletion of the Chrnb4 gene did not influence ethanol or sucrose consumption in the DID paradigm (Fig. 3). Data from the DID procedure were analyzed for the final 4 h ethanol or sucrose session [30]. Additionally, the blood ethanol concentration at the end of the 4 h session was analyzed. All 3 dependent variables were analyzed using a 2-way ANOVA with sex and strain included as independent variables. There were no significant main effects or interactions observed for any dependent variable.Fig. 3


No evidence of a role of the β 4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors
Deletion of the Chrnb4 gene does not modulate binge-like ethanol consumption. Data (mean ± SEM) represent 4 h ethanol consumption (a), BEC after 4 h ethanol intake (b), and 4 h sucrose consumption (c). Female WT = 6, HET = 7, KO = 6; Male WT = 5, HET = 6, KO = 4
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Related In: Results  -  Collection

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Fig3: Deletion of the Chrnb4 gene does not modulate binge-like ethanol consumption. Data (mean ± SEM) represent 4 h ethanol consumption (a), BEC after 4 h ethanol intake (b), and 4 h sucrose consumption (c). Female WT = 6, HET = 7, KO = 6; Male WT = 5, HET = 6, KO = 4
Mentions: Deletion of the Chrnb4 gene did not influence ethanol or sucrose consumption in the DID paradigm (Fig. 3). Data from the DID procedure were analyzed for the final 4 h ethanol or sucrose session [30]. Additionally, the blood ethanol concentration at the end of the 4 h session was analyzed. All 3 dependent variables were analyzed using a 2-way ANOVA with sex and strain included as independent variables. There were no significant main effects or interactions observed for any dependent variable.Fig. 3

View Article: PubMed Central - PubMed

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.

Electronic supplementary material: The online version of this article (doi:10.1186/s13104-017-2470-7) contains supplementary material, which is available to authorized users.

No MeSH data available.