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Psychological Science
Completed Project

Auditory Fear Conditioning in a Mouse Model of Fragile X Syndrome (FXS)

Alexander Koo ’18 and Bojana Zupan (Pscyhology)

Sociability varies widely among individuals and depends on a number of developmental factors. As social animals, mice are a good model for studying sociability and the factors that affect it. Mice modeling Fragile X Syndrome (FXS), a genetic mutation-induced condition characterized by intellectual disability and social anxiety, display abnormal sociability. Yet previous research in our lab found that abnormal sociability is not only dependent on the organism’s genotype, but also on that of its mother. This suggests that sociability may be developmentally programmed by nongenetic factors. Sociability is in part regulated by the amygdala as inhibition of certain amygdaloid projections increases social interaction in mice. In FXS mice, defects in synaptic plasticity and neurotransmission in the amygdala have also been reported. We therefore asked whether increased sociability observed in our mice is associated with maternal genotype-dependent changes in amygdala function. Using cued fear conditioning, a classical amygdala-dependent learning task, we assessed whether maternal or offspring FXS mutation alters acquisition and/or extinction of fear memory. We found no effect of maternal nor, surprisingly, offspring’s own genotype on fear learning. This finding fails to replicate published data showing deficits in expression of fear memory in FXS mice. However, differing mouse strains may explain our inability to replicate these results as our mouse has very low if any freezing behavior in response to fear conditioning. We are currently reassessing our results using locomotor activity as a behavioral measure of fear learning. If our findings are confirmed, the lack of differences in fear learning would suggest that abnormal sociability is not mediated by amygdala dysfunction. However, we can’t rule out the possibility that the indiscriminate social approach observed in our mice may be at least in part mediated by a more nuanced deficit in processing of aversive social cues.