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HERO ID
2284021
Reference Type
Journal Article
Title
Sodium butyrate into the insular cortex during conditioned taste-aversion acquisition delays aversive taste memory extinction
Author(s)
Núñez-Jaramillo, L; Reyes-López, J; Miranda, MI
Year
2014
Is Peer Reviewed?
1
Journal
NeuroReport
ISSN:
0959-4965
EISSN:
1473-558X
Volume
25
Issue
6
Page Numbers
386-390
Language
English
PMID
24323127
DOI
10.1097/WNR.0000000000000103
Abstract
Histone acetylation is one mechanism that promotes gene expression, and it increases during learning of various tasks. Specifically, novel taste consumption produces an increased acetylation of histone lysine residues in the insular cortex (IC), where protein synthesis is crucial during memory consolidation of conditioned taste aversion (CTA). However, the role of this elevated histone acetylation during CTA learning has not been examined directly. Thus, the present study investigated the effects of sodium butyrate (NaBu), a histone deacetylase inhibitor, injected into the IC during CTA acquisition. Male Wistar rats, IC bilaterally implanted, were injected 60 min before saccharine presentation, with a total volume of 0.5 µl of NaBu solution (100, 500, and 10 µg/0.5 µl) or saline; 30 min later animals were injected intraperitoneally with lithium chloride, a malaise-inducing drug. The next day, CTA retrieval was tested. No effects of NaBu were observed during acquisition or retrieval, but during extinction trials, a significant delay in aversive memory extinction was observed in the group injected with the lowest NaBu dose. This result indicates that NaBu in the IC strengthens CTA and delays aversive memory extinction, and suggests that histone acetylation could increase long-term taste-aversive memory strength.
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n-Butanol
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