Social defeat leads to selective avoidance of familiar opponents as well as general avoidance of novel, non-threatening intruders. Avoidance of familiar opponents represents a fear-related memory whereas generalized social avoidance indicates anxiety-like behavior. We have previously shown that
serotonin signaling alters responses to social defeat in Syrian hamsters, although it is unclear whether
serotonin modulates defeat-induced fear, anxiety, or both. In this study we focus on 5-HT1A receptors, in part, because their activation had been linked to the acquisition of conditioned fear. We hypothesized that pharmacological activation of 5-HT1A receptors prior to social defeat would reduce avoidance of familiar opponents and impair
Arc expression in the basolateral amygdala (BLA), but not alter anxiety-like behavior. We administered
8-OH-DPAT, a
5-HT1A receptor agonist, prior to 3, 5-minute social defeats and 24h later exposed hamsters to a social interaction test to measure the conditioned defeat response immediately followed by either a Y-maze test or an open field test. In a separate experiment, we administered
8-OH-DPAT prior to 3, 5-minute social defeats and later removed the brains for
Arc immunohistochemistry. Social defeat increased the number of
Arc immunopositive cells in the central amygdala (CeA), prelimbic cortex (PL), and BLA, and
8-OH-DPAT treatment reduced
Arc immunoreactivity in the PL. These results suggest that
5-HT1A receptor activation impairs the fear memory associated with social defeat, but does not alter defeat-induced anxiety. Overall,
5-HT1A receptor activation may impair
Arc expression in select brain regions such as the PL and thereby disrupt the development of a fear memory essential for the conditioned defeat response.