Raul Ramos
Turrigiano Lab
“The role of homeostatic plasticity in associative learning and memory”
The taste system can be a powerful choice when studying the mechanisms of learning. Model animals such as rats can develop a learned aversion to a taste after only one bout of illness following delivery of that taste. Mr. Ramos gave evidence for how a homeostatic (balancing) mechanism called synaptic scaling is made by taste cortex during learning and memory formation.
A central goal of neuroscience research is to advance our understanding of the cellular physiology underlying learning and memory processes. The most extensively studied model for how associative learning is achieved at the cellular level is the Hebbian modification of synapses. However, computational modeling studies have demonstrated that these forms of plasticity follow positive feedback rules, making them inherently destabilizing in nature. Without additional features, Hebbian plasticity could give way to “unconstrained” synaptic strengthening. Homeostatic synaptic plasticity (HSP) is hypothesized to be the basis for neural-network stability during learning-driven changes of synaptic strength. Synaptic scaling, the most extensively studied form of HSP, is hypothesized to constrain the positive feedback nature of Hebbian plasticity while simultaneously preserving circuit features permissive to learning. Despite its potential impact on our current understanding of associative learning processes, this hypothesis remains untested and the consequences of disrupted synaptic scaling on learning remain unknown. This project aims to determine the role of homeostatic synaptic scaling in associative learning and memory using a conditioned taste aversion (CTA) paradigm in rats. First, we demonstrate that synaptic scaling can be engaged by neurons in the gustatory cortex in response to activity perturbation. Second, we extensively characterized an understudied phenomenon within CTA learning known as CTA induced generalized aversion. Lastly, we show that virus mediated delivery of synaptic scaling blockers enhances the persistence of the generalized aversion. Taken together, these results demonstrate that homeostatic synaptic plasticity plays a role in maintaining memory specificity and preventing the persistence of generalization.