Abstract
Alcohol use disorder (AUD) is a significant global health issue. Despite historically higher rates among men, AUD prevalence and negative alcohol-related outcomes in women are rising. Loneliness in humans has been associated with increased alcohol use, and traditional rodent drinking models involve single housing, presenting challenges for studying social enrichment. We developed LIQ PARTI (Lick Instance Quantifier with Poly-Animal RFID Tracking Integration), an open-source tool to examine home cage continuous access two-bottle choice drinking behavior in a group-housed setting, investigating the influence of sex and social isolation on ethanol consumption and bout microstructure in C57Bl/6J mice. LIQ PARTI, based on our previously developed single-housed LIQ HD system, accurately tracks drinking behavior using capacitive-based sensors and RFID technology. Group-housed female mice exhibited higher ethanol preference than males, while males displayed a unique undulating pattern of ethanol preference linked to cage changes, suggesting a potential stress or novelty-related response. Chronic ethanol intake distinctly altered bout microstructure between male and female mice, highlighting sex and social environmental influences on drinking behavior. Social isolation with the LIQ HD system amplified fluid intake and ethanol preference in both sexes, accompanied by sex- and fluid-dependent changes in bout microstructure. However, these effects largely reversed upon resocialization, indicating the plasticity of these behaviors in response to social context. Utilizing a novel group-housed home cage lickometer device, our findings illustrate the critical interplay of sex and housing conditions in voluntary alcohol drinking behaviors in C57Bl/6J mice, facilitating nuanced insights into the potential contributions to AUD etiology.
Footnotes
The authors declare no competing financial interests.
N.P. was supported by an F30 from the National Institute on Alcohol Abuse and Alcoholism (NIAAA; AA029599), a T32 from the National Institute of General Medical Sciences (NIGMS; GM007347), and an R01 Diversity Supplement from the National Institute of Neurological Disorders and Stroke (NINDS; NS102306-04S1).
D.N.A. was supported by an F31 from the NIAAA (AA030901). C.M.E. was supported by a T32 from the NIMH (MH065215). M.A.D. was supported by an F32 from the NIAAA (AA029592) and T32s from the NINDS and NIMH (NS007491 and MH065215). D.G.W. and the research were supported by an R37 from the NIAAA (AA019455) and P60 (AA031124).
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