Analysis of the role of 5-HT2aR as a target for enhanced social cognition and episodic memory.

NOELIA V WEISSTAUB; SACSON AGOSTINA; MORICI FACUNDO; BEKINSCHTEIN, PEDRO

san diego

Congreso; Neuroscience Meeting; 2018

Society for neuroscience

Social Cognition encloses a largevariety of behaviors and it is a domain commonly affected in psychiatricdisorders. Serotonin has been linked to social behavior in humans due to itsassociation with the regulation of mood and anxiety behaviors and also due to theuse of selective serotonin reuptake inhibitors as the first line of treatmentfor a large number of these disorders. Recently it has become clearer thatepisodic memory systems can interact with social cognitive processes and thatappropriate memory processing is important to navigate the social world.Interestingly, somebrain areas involved in social cognition overlap with theones involved in episodic memory. In this work we analyzed if chronic administration of the antidepressant fluoxetine (FLX)affects social interaction and memory processes and a putative role of 5-HT2aRin this effect. For this purpose, we administrated a chronic oral dose of FLX (10mg/kg) to wild type (WT) and 5-HT2aR knockout mice (KO). After 4 weeks of FLXadministration, the animals performed a series of behavioral tasks that includenovelty suppressed feeding (NSF), social interaction (SI) and novel objectrecognition ( NOR). We used a NOR task with a 3 min training session that was notenough to generate a long-term NOR memory at 24 h in WT or KO mice.Interestingly, after FLX treatment WT but not KO mice remembered having seenthe familiar object during a test performed 24 h after training. We observed nointeraction between genotype and treatment when mice were trained to generate along.term memory. In the social interaction task, chronic FLX increased theexploration time of the social stimuli in WT but not in KO mice. These resultssuggest that chronic fluoxetine can influence social interaction andepisodic like memory and that these effects are at least partially mediated by5-HT2aR.