Figure 3.

Mice escape more rapidly (mean latency ± SEM) from the SAM apparatus / SAM social interactions with familiarity, which is enhanced by anxiolytic treatments, and inhibited by anxiogenic treatments. A) Mice injected icv with neuropeptide S (NPS, dashed line with circles) escape significantly faster from the SAM open field (OF) alone (in the absence of social interaction) than aCSF treated controls (solid line/triangles) on the initial trial (#) and during trials on days 3 and 4 (*). B) Mice given access to exercise (running wheel, dashed line/circles) exhibit reduced latency to escape from social aggression on the initial (*) and 3^rd trials (#) of SAM social interaction compared to animals that received aggression in the absence of the opportunity for voluntary exercise (solid line/triangles). C) Escaping mice injected ip with the anxiogenic α₂-adrenoreceptor antagonist yohimbine on day 3 of SAM social interaction, but continued to escape (See Fig. 3A), did so significantly more slowly (*) on day 3 than mice injected with vehicle. D) Non-escaping submissive mice injected ip with the anxiolytic CRF₁ receptor antagonist antalarmin that began escaping (See Fig. 3B) on day 3 did so significantly more rapidly in initial escape (*) than the initial escape (day 1) of escaping animals injected with vehicle, but more slowly than vehicle controls escaped on day 3.