EXTINCTION OF CONDITIONED TASTE AVERSION INDUCES METAPLASTIC MODULATION OF IN VIVO LONG-TERM DEPRESSION IN THE INSULAR CORTEX

Memory formation and extinction rely on dynamic changes in synaptic plasticity that are tightly regulated by homeostatic mechanisms. Metaplasticity adjusts the thresholds for synaptic modification as a function of prior neuronal activity. Our previous work demonstrated that conditioned taste aversion (CTA) training blocks the expression of both long-term potentiation (LTP) and long-term depression (LTD) in vivo within the basolateral amygdala–insular cortex (BLA–IC) pathway. However, whether the behavioral attenuation of the aversive memory during extinction is accompanied by a recovery of synaptic plasticity, particularly LTD in vivo, remains unclear. We demonstrate that CTA extinction both partially restores LTD expression in the BLA–IC pathway and reverts the associated CTA-induced increase in synaptic excitability. This restoration of synaptic plasticity is accompanied by a significant decrease in insular cortex brain-derived neurotrophic factor (BDNF) levels following extinction, compared to animals that retained the aversive memory. These results indicate that extinction modulates synaptic plasticity in the BLA–IC pathway, counteracting the LTD suppression and excitability changes induced by aversive memory, and suggest that BDNF downregulation accompany these metaplastic changes.