| First Author | Kamens HM | Year | 2017 |
| Journal | BMC Res Notes | Volume | 10 |
| Issue | 1 | Pages | 151 |
| PubMed ID | 28381286 | Mgi Jnum | J:242831 |
| Mgi Id | MGI:5906936 | Doi | 10.1186/s13104-017-2470-7 |
| Citation | Kamens HM, et al. (2017) No evidence of a role of the beta4 subunit of the nicotinic acetylcholine receptor in alcohol-related behaviors. BMC Res Notes 10(1):151 |
| abstractText | BACKGROUND: Nicotinic acetylcholine receptors have gained attention in the last several years as mediators of alcohol-related behaviors. The genes that code for the alpha5, alpha3, and beta4 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 beta4 subunit is not involved in mediating these responses. CONCLUSIONS: While we found no evidence for the involvement of the beta4 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. |
