BDNF reverses the CTA memory deficits produced by inhibition of protein synthesis.

Brain-derived neurotrophic factor (BDNF) is an essential protein synthesis product that has emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Our previous studies on the insular cortex (IC), a region of the temporal cortex implicated in the acquisition and storage of conditioned taste aversion (CTA), have demonstrated that intracortical microinfusion of BDNF induces a lasting potentiation of synaptic efficacy in the projection from the basolateral nucleus of the amygdala (Bla) to the IC of adult rats in vivo. Recently, we found that intracortical microinfusion of BDNF previous to CTA training enhances the retention of this task. In this work, we present experimental data showing that acute intracortical delivery of BDNF (2 microg/2 microl per side) reverses the deficit in CTA memory caused by inhibition of insular cortex protein synthesis due to anisomycin administration (100 microg/microl per side) in male adult Wistar rats. These findings suggest that BDNF is a protein synthesis product essential for neocortical long-term memory storage.