Abstract
All associative learning is a balance between the specific details of a memory and what can be generalized to future scenarios. While the mechanisms for memory acquisition have been studied for decades, the synaptic plasticity that shapes the generalization of memory is less well characterized. In this thesis, I present results that define the underlying synaptic plasticity mechanisms that govern two distinct types of aversive memory generalization: a transient and a long-lasting generalized aversion. Using conditioned taste aversion (CTA) as a model learning paradigm, my collaborators and I found that following moderate CTA conditioning (0.15M LiCl) animals form a transient generalized aversion that dissipates within 24 hours. This momentary generalized aversion is supported by a transient increase in post-synaptic strengths that is homeostatically scaled down. On the other hand, the long-lasting generalized aversion resulting from strong CTA conditioning (0.30M LiCl) persists up to two-weeks post-conditioning. This persistence is supported by a parallel long-lasting increase in post-synaptic strength. Exposure to the generalized tastant drives reversal of both the generalized aversion and the increase in post-synaptic strength. Finally, these dynamic changes in synaptic strength take place within the conditioning-active ensemble without impacting the retrieval of CTA memory, suggesting that the maintenance of CTA memory may rely on a different population of cells following acquisition. These results highlight novel synaptic plasticity mechanisms of memory generalization.