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Oxytocin increases the salience of both positive and negative social contexts and it is thought that these diverse actions on behavior are mediated in part through circuit-specific action. This hypothesis is based primarily on manipulations of oxytocin receptor function, leaving open the question of whether different populations of oxytocin neurons mediate different effects on behavior. Here we inhibited oxytocin synthesis in a stress-sensitive population of oxytocin neurons specifically within the medioventral bed nucleus of the stria terminalis (BNSTmv). Oxytocin knockdown prevented social stress-induced increases in social vigilance and decreases in social approach. Viral tracing of BNSTmv oxytocin neurons revealed fibers in regions controlling defensive behaviors, including lateral hypothalamus, anterior hypothalamus, and anteromedial BNST (BNSTam). Oxytocin infusion into BNSTam in stress naïve mice increased social vigilance and reduced social approach. These results show that a population of extrahypothalamic oxytocin neurons plays a key role in controlling stress-induced social anxiety behaviors.

Background: Preclinical evidence from male subjects indicates that exposure to psychotropic medications, during early development, results in long-lasting altered responses to reward-related stimuli. However, it is not known if exposure to the antidepressant fluoxetine, in female subjects specifically, changes sensitivity to natural and drug rewards, later in life.Aims: The aim of this work was to investigate if exposure to fluoxetine mediates enduring changes in sensitivity to the rewarding properties of cocaine and sucrose, using female mice as a model system.Methods: We exposed C57BL/6 female mice to fluoxetine (250 mg/L in their drinking water) for 15 consecutive days, either during adolescence (postnatal day 35-49) or adulthood (postnatal day 70-84). Twenty-one days later, mice were examined on their behavioral reactivity to cocaine (0, 2.5, 5, 7.5 mg/kg) using the conditioned place preference paradigm, or assessed on the two-bottle sucrose (1%) test.Results: We found that regardless of age of antidepressant exposure, female mice pre-exposed to fluoxetine displayed reliable conditioning to the cocaine-paired compartment. However, when compared to respective age-matched controls, antidepressant pre-exposure decreased the magnitude of conditioning at the 5 and 7.5 mg/kg cocaine doses. Furthermore, fluoxetine pre-exposure reduced sucrose preference without altering total liquid intake.Conclusions: The data suggest that pre-exposure to fluoxetine, during adolescence or adulthood, results in a prolonged decrease in sensitivity to the rewarding properties of both natural and drug rewards in female C57BL/6 mice. [ABSTRACT FROM AUTHOR]

Anxiety-related illnesses constitute one of the leading causes of disability across the globe. Consequently, the need for validated preclinical models to uncover the etiology of anxiety phenotypes remains essential. Given the link between social stress experience and the manifestation of anxiogenic-like outcomes, we evaluated whether social defeat stress (SDS) reduces open-space exploratory behavior in prairie voles ( Microtus ochrogaster ). Thus, we exposed adult sexually-naïve male voles to 10 consecutive days of SDS episodes and evaluated responses to the anxiogenic environment of the light/dark box test or the elevated plus-maze, 24 hours later. We found that, when compared to non-stressed controls, SDS-exposed voles displayed longer latency to enter the light compartment of the light/dark box. Similarly, on the elevated plus-maze, SDS-exposed voles displayed decreases in the number of entries into the open arms, while spending more time in the closed arms of the maze. No differences in locomotor activity were noted between the experimental groups. Collectively, these data indicate that chronic SDS exposure induces anxiety-like responses in adult male prairie voles, thus, providing a preclinical model for the study of social stress-induced anxiogenic phenotypes., Competing Interests: None declared., (© The Author(s) 2024. Published by Oxford University Press.)