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Drinking alcohol is facilitated by social interactions with peers, especially during adolescence. The importance of peer social influences during adolescence on alcohol and substance use has recently received more attention. We have shown that social interaction with an alcohol‐intoxicated peer influences adolescent alcohol drinking differently in male and female rats using the demonstrator–observer paradigm. The present set of experiments analyzed the social interaction session to determine changes in social behaviors and subsequent alcohol drinking in adolescent male and female rats. Specifically, in Experiment 1, we determined whether specific social behaviors were altered during interaction with an alcohol‐intoxicated demonstrator administered 1.5 g/kg ethanol (EtOH) and assessed changes in EtOH intake in adolescent observers. Experiment 2 examined changes in voluntary saccharin consumption to determine whether social interaction with an alcohol‐intoxicated demonstrator administered 1.5 g/kg EtOH altered consumption of a palatable solution. In Experiment 3, we administered saline, and a low (5 mg/kg) or high (20 mg/kg) dose of cocaine to the demonstrator and assessed changes in the adolescent observers to determine whether social interaction with a “drugged” peer altered social behaviors and voluntary EtOH intake. We showed that social interaction with an alcohol‐intoxicated demonstrator administered 1.5 g/kg EtOH (i) decreased social play and increased social investigation and social contact in adolescent male and female observers, (ii) did not alter nonsocial behaviors, (iii) did not alter saccharin consumption, and (iv) increased voluntary EtOH intake in adolescent female but not male observers. When the peer was injected with cocaine, (i) social play was dose‐dependently decreased, (ii) there were no changes in other social or nonsocial behaviors, and (iii) voluntary EtOH intake in adolescent male and female observers was unaffected. The present results are consistent and extend our previous work, showing that social interaction with an alcohol‐intoxicated peer selectively alters social behaviors and alcohol drinking in adolescent rats. Females appear to be more sensitive to the elevating effects of social interaction on voluntary EtOH consumption. Drinking alcohol is facilitated by social interactions with peers, especially during adolescence. The present research aimed to determine changes in social behaviors and ethanol consumption following interaction with an alcohol‐intoxicated or cocaine‐injected peer in adolescent male and female rats. Social interaction with an alcohol‐intoxicated peer altered social behaviors. Only females showed increased ethanol consumption following interaction with an alcohol‐intoxicated peer. The present results show that interaction with an alcohol‐intoxicated peer selectively alters social behaviors and alcohol‐drinking in adolescent rats.

ABSTRACTWhile direct contact may sometimes be sufficient to allow a pathogen to jump into a new host species, in other cases, fortuitously adaptive mutations that arise in the original donor host are also necessary. Viruses have been the focus of most host shift studies, so less is known about the importance of ecological versus evolutionary processes to successful bacterial host shifts. Here we tested whether direct contact with the novel host was sufficient to enable the mid-1990s jump of the bacterium Mycoplasma gallisepticumfrom domestic poultry to house finches (Haemorhous mexicanus). We experimentally inoculated house finches with two genetically distinct M. gallisepticumstrains obtained either from poultry (Rlow) or from house finches (HF1995) during an epizootic outbreak. All 15 house finches inoculated with HF1995 became infected, whereas Rlow successfully infected 12 of 15 (80%) inoculated house finches. Comparisons among infected birds showed that, relative to HF1995, Rlow achieved substantially lower bacterial loads in the host respiratory mucosa and was cleared faster. Furthermore, Rlow-infected finches were less likely to develop clinical symptoms than HF1995-infected birds and, when they did, displayed milder conjunctivitis. The lower infection success of Rlow relative to HF1995 was not, however, due to a heightened host antibody response to Rlow. Taken together, our results indicate that contact between infected poultry and house finches was not, by itself, sufficient to explain the jump of M. gallisepticumto house finches. Instead, mutations arising in the original poultry host would have been necessary for successful pathogen emergence in the novel finch host.