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

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.


Deletion of the Chrnb4 gene did not influence ethanol-induced ataxia measured on the dowel test. Data (mean ± SEM) represent the latency to fall from the dowel (a) immediately or (b) 30 min after a 1.5 g/kg ethanol injection. Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 7, KO = 8
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Fig5: Deletion of the Chrnb4 gene did not influence ethanol-induced ataxia measured on the dowel test. Data (mean ± SEM) represent the latency to fall from the dowel (a) immediately or (b) 30 min after a 1.5 g/kg ethanol injection. Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 7, KO = 8

Mentions: Similar to results with the balance beam, deletion of the Chrnb4 gene also did not influence ataxia as measured on the dowel test (Fig. 5). Two mice did not reach training criteria (2 min on the dowel; 1 HET, 1 KO) and were excluded from ethanol testing. There were no statistically significant differences between β4 WT, HET, or KO mice immediately following the ethanol injection or 30 min later on the dowel test when analyzed with a Kruskal–Wallis test.Fig. 5


No evidence of a role of the β 4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors
Deletion of the Chrnb4 gene did not influence ethanol-induced ataxia measured on the dowel test. Data (mean ± SEM) represent the latency to fall from the dowel (a) immediately or (b) 30 min after a 1.5 g/kg ethanol injection. Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 7, KO = 8
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC5382442&req=5

Fig5: Deletion of the Chrnb4 gene did not influence ethanol-induced ataxia measured on the dowel test. Data (mean ± SEM) represent the latency to fall from the dowel (a) immediately or (b) 30 min after a 1.5 g/kg ethanol injection. Female WT = 9, HET = 8, KO = 10; Male WT = 8, HET = 7, KO = 8
Mentions: Similar to results with the balance beam, deletion of the Chrnb4 gene also did not influence ataxia as measured on the dowel test (Fig. 5). Two mice did not reach training criteria (2 min on the dowel; 1 HET, 1 KO) and were excluded from ethanol testing. There were no statistically significant differences between β4 WT, HET, or KO mice immediately following the ethanol injection or 30 min later on the dowel test when analyzed with a Kruskal–Wallis test.Fig. 5

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.