Background: Peer drinking is one of the most robust predictors of college students' alcohol use and can moderate students' genetic risk for alcohol use. Peer effect research generally suffers from 2 problems: selection into peer groups and relying more on perceptions of peer alcohol use than peers' selfreport. The goal of the present study was to overcome those limitations by capitalizing on a genetically informed sample of randomly assigned college roommates to examine multiple dimensions of peer influence and the interplay between peer effects and genetic predisposition on alcohol use, in the form of polygenic scores.Methods: We used a subsample (n = 755) of participants from a university-wide, longitudinal study at a large, diverse, urban university. Participants reported their own alcohol use during fall and spring and their perceptions of college peers' alcohol use in spring. We matched individuals into their rooms and residence halls to create a composite score of peer-reported alcohol use for each of those levels. We examined multiple dimensions of peer influence and whether peer influence moderated genetic predisposition to predict college students' alcohol use using multilevel models to account for clustering at the room and residence hall level.Results: We found that polygenic scores (b = 0.12), perceptions of peer drinking (b = 0.37), and roommates' self-reported drinking (b = 0.10) predicted alcohol use (all ps < 0.001), while average alcohol use across residence hall did not (b = À0.01, p = 0.86). We found no evidence for interactions between peer influence and genome-wide polygenic scores for alcohol use.Conclusions: Our findings underscore the importance of genetic predisposition on individual alcohol use and support the potentially causal nature of the association between peer influence and alcohol use.

Adolescence is characterized by high levels of playful social interaction, cognitive development, and increased risk-taking behavior. Juvenile exposure to social isolation or social stress can reduce myelin content in the frontal cortex, alter neuronal excitability, and disrupt hypothalamic pituitary adrenal (HPA) axis function. As compared to group housed animals, social isolation increases anxiety-like phenotypes and reduces social and cognitive performance in adulthood. We designed a neighbor housing environment to alleviate issues related to social isolation that still allowed individual homecages. Neighbor housing consists of four standard mouse cages fused together with semi-permeable ports that allow visual, olfactory, and limited social contact between mice. Adolescent C57BL/6J males and females were group housed (4/cage), single housed (1/cage), or neighbor housed (4/complex). As adults, mice were tested for social, anxiety-like, and cognitive behaviors. Living in this neighbor environment reduced anxiety-like behavior in the social interaction task and in the light-dark task. It also rescued cognitive deficits from single housing in the novel object recognition task. These data suggest that neighbor housing may partially ameliorate the social anxiety and cognitive deficits induced by social isolation. These neighbor cage environments may serve as a conduit by which researchers can house mice in individual cages while still enabling limited social interactions to better model typical adolescent development.

Background: Trauma related psychiatric disorders, such as posttraumatic stress disorder (PTSD), and alcohol use disorder (AUD) are highly comorbid illnesses that separately present an opposing, sex-specific pattern, with increased prevalence of PTSD in females and increased prevalence of AUD diagnoses in males. Likewise, PTSD is a risk factor in the development of AUD, with conflicting data on the impact of sex in the comorbid development of both disorders. Because the likelihood of experiencing more than one traumatic event is high, we aim to utilize chronic repeated predatory stress (CRPS) to query the extent to which sex interacts with CRPS to influence alcohol consumption, or cessation of consumption.Methods: Male (n=16) and female (n=15) C57BL/6J mice underwent CRPS or daily handling for two weeks during adolescence (P35-P49) and two weeks during adulthood (P65-P79). Following the conclusion of two rounds of repeated stress, behavior was assessed in the open field. Mice subsequently underwent a two-bottle choice intermittent ethanol access (IEA) assessment (P90-131) with the options of 20% ethanol or water. After establishing drinking behavior, increasing concentrations of quinine were added to the ethanol to assess the drinking response to adulteration of the alcohol. Results: CRPS increased fecal corticosterone concentrations and anxiety-likebehaviors in the open field in both male and female mice as compared to control mice that had not been exposed to CRPS. Consistent with previous reports, we observed a sex difference in alcohol consumption such that females consumed more ethanol per gram of body mass than males. In addition, CRPS reduced alcohol aversion in male mice such that higher concentrations of quinine were necessary to reduce alcohol .

Because EtOH sensitivity is predictive of risk of developing AUD in humans, our data indicate that dietary LC ω-3 levels should be evaluated for their impact on AUD risk in humans. Further, these studies indicate that genetic background can interact with fatty acids in the diet to significantly alter EtOH-responsive behaviors.

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