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Overcoming specific fears and subsequent anxiety can be greatly enhanced by the presence of familiar social partners, but the neural circuitry that controls this phenomenon remains unclear. To overcome this, the social interaction (SI) habituation test was developed in this lab to systematically investigate the effects of social familiarity on anxiety-like behavior in rats. Here, we show that social familiarity selectively reduced anxiety-like behaviors induced by an ethological anxiogenic stimulus. The anxiolytic effect of social familiarity could be elicited over multiple training sessions and was specific to both the presence of the anxiogenic stimulus and the familiar social partner. In addition, socially familiar conspecifics served as a safety signal, as anxiety-like responses returned in the absence of the familiar partner. The expression of the social familiarity-induced anxiolysis (SFiA) appears dependent on the prefrontal cortex (PFC), an area associated with cortical regulation of fear and anxiety behaviors. Inhibition of the PFC, with bilateral injections of the GABAA agonist muscimol, selectively blocked the expression of SFiA while having no effect on SI with a novel partner. Finally, the effect of D-cycloserine, a cognitive enhancer that clinically enhances behavioral treatments for anxiety, was investigated with SFiA. D-cycloserine, when paired with familiarity training sessions, selectively enhanced the rate at which SFiA was acquired. Collectively, these outcomes suggest that the PFC has a pivotal role in SFiA, a complex behavior involving the integration of social cues of familiarity with contextual and emotional information to regulate anxiety-like behavior. [ABSTRACT FROM AUTHOR]

Abstract: Certain serotonergic compounds that have an agonist/antagonist activity at the 5-HT1A receptor subtype are known to greatly potentiate the ability of light to advance the phase of circadian activity rhythms in hamsters. Typically, investigational compounds are injected 30 min to 1 h prior to a phase-advancing light pulse, and it is not known if these compounds are efficacious when injected after a short light pulse. In this study we injected the 5-HT1A mixed agonist/antagonist BMY 7378 from 1 to 7 h after a short phase advancing light pulse at CT 19 in hamsters to assess the temporal window of efficacy of this compound. BMY 7378 effectively doubles the magnitude of light-induced phase advances in hamster circadian wheel running rhythms for 6 h after a light pulse administered at CT 19, and this effect abruptly ends at 7 h post-light. This demonstrates that the molecular events initiated by a light pulse at CT 19 responsible for initiating phase advances in circadian activity rhythms can be modulated for at least the next 6 h in the hamster. However, this effect found with BMY 7378 does not extend to all serotonergic compounds as the inhibitory activity of 8-OH-DPAT on light-induced phase advances is not apparent when injected just 3 h after a light pulse. Since BMY 7378 can elicit such major shifts in the timing of the circadian clock it should be useful as a tool to explore potential changes in gene expression that lead to phase shifts in circadian rhythms, now known to be susceptible to modification for 6 h after a phase-advancing light pulse. [Copyright &y& Elsevier]