Late Protein Synthesis-Dependent Phases in CTA Long-Term Memory: BDNF Requirement

• Published in: Frontiers in behavioral neuroscience Vol. 5; p. 61
• Main Authors: Martínez-Moreno, Araceli, Rodríguez-Durán, Luis F, Escobar, Martha L
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Research Foundation 22.09.2011; Frontiers Media S.A
• Subjects: Anisomycin; BDNF; Brain-derived neurotrophic factor; Cortex (insular); CTA; Hippocampus; IC protein; insular cortex; Kinases; Laboratory animals; Long term memory; Long-term potentiation; Memory; memory persistence; Neuroscience; Protein biosynthesis; Protein synthesis; Proteins; Synaptic plasticity; Taste aversion; Temporal cortex; St Louis Missouri; United States > US; CTA; protein synthesis; insular cortex; BDNF; memory persistence
• ISSN: 1662-5153; 1662-5153
• DOI: 10.3389/fnbeh.2011.00061

It has been proposed that long-term memory (LTM) persistence requires a late protein synthesis-dependent phase, even many hours after memory acquisition. Brain-derived neurotrophic factor (BDNF) is an essential protein synthesis product that has emerged as one of the most potent molecular mediators for long-term synaptic plasticity. Studies in the rat hippocampus have been shown that BDNF is capable to rescue the late-phase of long-term potentiation as well as the hippocampus-related LTM when protein synthesis was inhibited. 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 delivery of BDNF reverses the deficit in CTA memory caused by the inhibition of IC protein synthesis due to anisomycin administration during early acquisition. In this work, we first analyze whether CTA memory storage is protein synthesis-dependent in different time windows. We observed that CTA memory become sensible to protein synthesis inhibition 5 and 7 h after acquisition. Then, we explore the effect of BDNF delivery (2 μg/2 μl per side) in the IC during those late protein synthesis-dependent phases. Our results show that BDNF reverses the CTA memory deficit produced by protein synthesis inhibition in both phases. These findings support the notion that recurrent rounds of consolidation-like events take place in the neocortex for maintenance of CTA memory trace and that BDNF is an essential component of these processes.