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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.


Metabolism of an acute injection of ethanol (3 g/kg) is not influence by the Chrnb4 gene. Data (mean ± SEM) represent blood ethanol concentrations (BEC). Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 6, KO = 8
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Fig7: Metabolism of an acute injection of ethanol (3 g/kg) is not influence by the Chrnb4 gene. Data (mean ± SEM) represent blood ethanol concentrations (BEC). Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 6, KO = 8

Mentions: Ethanol metabolism was not influenced by the absence of the Chrnb4 gene (Fig. 7). BEC from 30, 60 120, and 180 min after an acute 3 g/kg ethanol injection was examined with a repeated measures ANOVA. A significant main effect of time (F3, 129 = 420.2, p < 0.001) was observed, but no other significant main effects or interactions. As expected BEC levels decreased from the time of injection. Importantly, genotype did not influence ethanol metabolism. Raw data of all experiments are found in supplementary materials (Additional file 3).Fig. 7


No evidence of a role of the β 4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors
Metabolism of an acute injection of ethanol (3 g/kg) is not influence by the Chrnb4 gene. Data (mean ± SEM) represent blood ethanol concentrations (BEC). Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 6, KO = 8
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
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getmorefigures.php?uid=PMC5382442&req=5

Fig7: Metabolism of an acute injection of ethanol (3 g/kg) is not influence by the Chrnb4 gene. Data (mean ± SEM) represent blood ethanol concentrations (BEC). Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 6, KO = 8
Mentions: Ethanol metabolism was not influenced by the absence of the Chrnb4 gene (Fig. 7). BEC from 30, 60 120, and 180 min after an acute 3 g/kg ethanol injection was examined with a repeated measures ANOVA. A significant main effect of time (F3, 129 = 420.2, p < 0.001) was observed, but no other significant main effects or interactions. As expected BEC levels decreased from the time of injection. Importantly, genotype did not influence ethanol metabolism. Raw data of all experiments are found in supplementary materials (Additional file 3).Fig. 7

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 &alpha;5, &alpha;3, and &beta;4 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 &beta;4 subunit is not involved in mediating these responses.

Conclusions: While we found no evidence for the involvement of the &beta;4 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.