Social support favors extinction and impairs acquisition of both short- and long-term contextual fear conditioning memory.

Fear memory has an essential role on animal's survival once it induces defensive behavior in response to threats. Among other factors, social support is known to down-regulate the expression of fear conditioned response, representing an important modulator of fear memories. Here we studied the effects of social support during acquisition, retrieval and extinction of contextual fear conditioning (CFC) memory in rats, by exposing the animals to the CFC task either in the absence or in the presence of a conspecific during the training, extinction and/or test sessions. The presence of a conspecific during the training session of CFC resulted in impairment to memory retention as verified in the short- and long-term memory test, suggesting that social support exerts a suppressive effect on the acquisition of CFC. On retrieval, social support decreased the expression of the conditioned fear response - as also seen in the extinction session. Nevertheless, the animals were able to learn the extinction memory as verified in the retention test. Therefore, this study demonstrates the effects of social support at crucial moments in CFC: impairing memory acquisition and favoring its extinction, by reducing the expression of the conditioned fear response with no impairment to the extinction learning.

Modulation of the storage of social recognition memory by neurotransmitter systems in the insular cortex.

The insular cortex (IC) receives projections from prefrontal, entorhinal and cingulate cortex, olfactory bulb and basal nuclei and has reciprocal connections with the amygdala and entorhinal cortex. These connections suggest a possible involvement in memory processes; this has been borne out by data on several behaviors. Social recognition memory (SRM) is essential to form social groups and to establish hierarchies and social and affective ties. Despite its importance, knowledge about the brain structures and the neurotransmitter mechanisms involved in its processing is still scarce. Here we study the participation of NMDA-glutamatergic, D1/D5-dopaminergic, H2-histaminergic, ß-adrenergic and 5-HT1A-serotoninergic receptors of the IC in the consolidation of SRM. Male Wistar rats received intra-IC infusions of substances acting on these receptors immediately after the sample phase of a social discrimination task and 24h later were exposed to a 5-min retention test. The intra-IC infusion of antagonists of D1/D5, ß-adrenergic or 5-HT1A receptors immediately after the sample phase impaired the consolidation of SRM. These effects were blocked by the concomitant intra-IC infusion of agonists of these receptors. Antagonists and agonists of NMDA and H2 receptors had no effect on SRM. The results suggest that the dopaminergic D1/D5, ß-adrenergic and serotonergic 5-HT1A receptors in the IC, but not glutamatergic NMDA and the histaminergic H2 receptors, participate in the consolidation of SRM in the IC.