Consolidation of an aversive taste memory requires two rounds of transcriptional and epigenetic regulation in the insular cortex

• Published in: Behavioural brain research 2019-01, Vol.356, p.371-374
• Main Authors: Rodríguez-Blanco, Luis Alfredo, Rivera-Olvera, Alejandro, Escobar, Martha L.
• Format: Article
• Language: English
• Subjects: Animals; Avoidance Learning - drug effects; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; Conditioning, Classical - drug effects; Conditioning, Classical - physiology; CTA; Epigenesis, Genetic - drug effects; Histone deacetylases; Insular cortex; Male; Memory - drug effects; Memory - physiology; Memory consolidation; Memory, Long-Term - drug effects; mRNA synthesis; Rats, Wistar; Taste - drug effects
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2018.09.009

•CTA-memory consolidation requires synthesis of new mRNA in the IC immediately and 7 h after acquisition of this task.•Inhibition of class I-type HDAC in the IC, immediately and 7 h after acquisition, converts a weak CTA into a strong one.•Memory consolidation of a strong CTA is not improved by the inhibition of class I-type HDAC in the IC. The current view of the neurobiology of learning and memory suggests that long-term memory (LTM) depends not only on the de novo protein synthesis but also on the synthesis of mRNA even hours after the acquisition of memory, as well as that the regulation of transcription through the histone acetylation is essential for the memory establishment. Our previous studies showed that protein synthesis inhibition around the time of training and 5–7 hours after acquisition in the insular cortex (IC) prevents the consolidation of conditioned taste aversion (CTA), a well-established learning and memory paradigm in which an animal learns to associate a novel taste with nausea. However, the participation of mRNA synthesis and the epigenetic regulation through histone acetylation in this process remains unexplored. In the present study we evaluated the effect of the inhibition of transcription as well as deacetylation of histones at two temporal windows on the consolidation of CTA. Thus, immediately or seven hours after CTA acquisition animals received a microinfusion of 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) or MS-275 in the IC, respectively. The present results show that transcription inhibition immediately and 7 h after acquisition impairs the CTA memory consolidation, whereas the inhibition of histone deacetylation strengths this memory at those temporal windows. These findings reveal that CTA memory requires recurrent rounds of transcriptional modulation events in the IC in order to consolidate this memory trace, demonstrating that transcriptional and epigenetic modulation substantially contribute to memory-consolidation-related functions performed by a neocortical area even several hours after memory acquisition.