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. 2020 Jul 3;10:11017. doi: 10.1038/s41598-020-67291-0

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Loss of NBCn1 increases alcohol consumption in mice. NBCn1 KO and WT mice (n = 10/group) were allowed free access to water and 3-15% alcohol for 4 days at each concentration, and alcohol consumption (A) and alcohol preference (B) were measured. Alcohol consumption was calculated as g of alcohol per kg body weight. Alcohol preference was calculated as percentage of alcohol over total fluid intake (water + alcohol). *p < 0.05 and **p < 0.01 compared to WT mice. (C) Schematic timeline for repeated episodes of alcohol withdrawal. Baseline consumption of 15% alcohol was first established in a two-bottle free choice procedure for 14 days and alcohol withdrawal was followed by 4 cycles of 6-day deprivation with 1-day access to alcohol. Alcohol consumption for 24 hrs was measured at the baseline (BL) and after withdrawal (WD1–4). (D) Alcohol consumption after repeated withdrawals (n = 10/group). *p < 0.05 compared to WT mice.