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

Epigenetic mechanisms regulate cue memory underlying discriminative behavior

“…A 2014 study by Nuñez-Jaramillo and colleagues ( Núñez-Jaramillo et al, 2014 ) found that infusing the general class I HDAC inhibitor, sodium butyrate (NaB), in the IC during CTA strengthened the associative memory between the taste cue and malaise, which was revealed behaviorally as delayed extinction of the taste aversion. The same effect of HDAC inhibition on CTA memory was also reported by ( Rodríguez-Blanco et al, 2019 ) with post-training IC injections of the HDAC1/3-selective inhibitor MS-275 (“entinostat”). In this study, the authors determined that at least two rounds of transcription – one immediately, and one 7 h after CTA acquisition – were needed to strengthen CTA memory consolidation for a specific flavor.…”

“…That said, effects on NOR do not appear to be limited to post-translational modifications since microRNAs also appear to play a role (e.g., Hansen et al, 2010 ). Interestingly, ‘strong’ training experiences are not affected by HDAC inhibitors that facilitate long-term memory formation following partial or weak training experiences ( Biergans et al, 2016 ; Heinrichs et al, 2013 ; McQuown and Wood, 2011 ; Merschbaecher et al, 2012 , 2016 ; Monsey et al, 2011 ; Stefanko et al, 2009 ; Rodríguez-Blanco et al, 2019 ), which suggests that when an experience-dependent threshold is reached, the system is no longer sensitive to further epigenetic perturbation. Overall, these findings implicate a variety of epigenetic modifications in the formation of memory that persists over longer periods of time.…”

Activity of Insula to Basolateral Amygdala Projecting Neurons is Necessary and Sufficient for Taste Valence Representation

“…Reciprocal connections of the anterior and posterior IC with the amygdala complex have been heavily implicated in rewardrelated encoding of both innate and learned (Stone et al, 2011;Jezzini et al, 2013;Haley et al, 2016). CTA acquisition results in a concerted bidirectional interplay of activity (Escobar and Bermú dez-Rattoni, 2000), posttranslation regulation (Adaikkan and Rosenblum, 2012), protein synthesis (Levitan et al, 2016;Guzmán-Ramos et al, 2018), as well as transcription and histone deacetylation (Rodríguez-Blanco et al, 2019), at the two regions. Though a number of gustatory relay stations undergo changes in activity and plasticity markers (Lamprecht and Dudai, 1995;Rosenblum et al, 1997;Swank, 1999), the aIC is unique in that its inactivation produces deficits in acquisition (Buresová, 1978;Gallo and Bures, 1991), and prominently suppresses CTA retrieval (Yasoshima et al, 2000;Yasoshima and Yamamoto, 2005;Gal-Ben-Ari and Rosenblum, 2011).…”