ArticlePharmacology, biochemistry, and behavior2013
The histone deacetylase inhibitor sodium butyrate modulates acquisition and extinction of cocaine-induced conditioned place preference.
Article in Pharmacology, biochemistry, and behavior, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Histone deacetylase inhibitor sodium butyrate increases risk-taking during acquisition of the rat gambling task.Psychopharmacology · 2026Article
- Microbiome-derived metabolites in substance use disorders: Mechanisms and implications.Annals of the New York Academy of Sciences · 2025Review
- Knockdown and overexpression of basolateral amygdala SIRT1 via AAV bidirectionally alter morphine-induced conditioned place preference extinction in mice.Frontiers in cellular neuroscience · 2025Article
- Beyond reconsolidation: The need for a broad theoretical approach in clinical translations of research on retrieval-induced plasticity.Behavioral neuroscience · 2024Review
- Review
- Sensory cortical and subcortical auditory neurophysiological changes predict cue-specific extinction behavior enabled by the pharmacological inhibition of an epigenetic regulator during memory formation.Brain research bulletin · 2021Article
- Evidence for Modulation of Substance Use Disorders by the Gut Microbiome: Hidden in Plain Sight.Pharmacological reviews · 2021Review
- Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020Review
- Behavioral and immunohistochemical characterization of rapid reconditioning following extinction of contextual fear.Learning & memory (Cold Spring Harbor, N.Y.) · 2019Article
- Epigenetic regulation of motivated behaviors by histone deacetylase inhibitors.Neuroscience and biobehavioral reviews · 2019Review
- Histone deacetylase inhibition differentially attenuates cue-induced reinstatement: An interaction of environment and acH3K9 expression in the dorsal striatum.Behavioral neuroscience · 2019Article
- Effects of a histone deacetylase 3 inhibitor on extinction and reinstatement of cocaine self-administration in rats.Psychopharmacology · 2019Article
- Involvement of the dorsal hippocampus in expression and extinction of cocaine-induced conditioned place preference.Hippocampus · 2018Article
- Persistent histone modifications at the BDNF and Cdk-5 promoters following extinction of nicotine-seeking in rats.Genes, brain, and behavior · 2018Article
- G Protein-Gated Inwardly Rectifying Potassium Channel Subunit 3 Knock-Out Mice Show Enhanced Ethanol Reward.Alcoholism, clinical and experimental research · 2016Article
- Medial prefrontal cannabinoid CB1 receptors modulate consolidation and extinction of cocaine-associated memory in mice.Psychopharmacology · 2015Article
- Inhibition of histone deacetylases facilitates extinction and attenuates reinstatement of nicotine self-administration in rats.PloS one · 2015Article
- Epigenetics and memory: causes, consequences and treatments for post-traumatic stress disorder and addiction.Genes, brain, and behavior · 2015Review
- Epigenetic mechanisms of memory formation and reconsolidation.Neurobiology of learning and memory · 2014Review
- Differential effects of dorsal hippocampal inactivation on expression of recent and remote drug and fear memory.Neuroscience letters · 2014Article
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5 authors.
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Abstract
Despite decades of research on treatments for cocaine dependence, relapse rates following many behavioral and drug-based therapies remain high. This may be in part because cocaine-associated cues and contexts can invoke powerful drug cravings years after quitting. Recent studies suggest that drugs that promote cognitive function can enhance the formation of memories involving cocaine and other substances. One target of these drugs is facilitating histone acetylation to promote learning by increasing gene transcription that supports memory formation. Here, we investigate the effects of the histone deacetylase (HDAC) inhibitor sodium butyrate (NaBut) on cocaine-induced conditioned place preference (CPP) in C57BL/6 mice. After establishing a graded dose-response curve (2, 5, & 20 mg/kg) for cocaine-induced CPP, we examined the effects of different doses of NaBut (0, 0.3, 0.6, & 1.2 g/kg) on conditioning, extinction, and post-extinction reconditioning of CPP. A high dose of NaBut (1.2 g/kg) enhanced initial acquisition of cocaine CPP, but there were no effects of NaBut on reconditioning of extinguished CPP. Effects of NaBut on extinction were more complex, with a low-dose (0.3 g/kg) facilitating extinction and a high dose (1.2 g/kg) weakening extinction evident by preference at a retention test. These findings suggest that HDAC inhibition may have dose dependent effects on different components of cocaine CPP, with implications for (1) involvement of histone acetylation in context-drug learning, (2) interpretation of acute and chronic drug effects, and (3) the targeting of different types of learning in therapeutic application of HDAC inhibitors.
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