ArticleLearning & memory (Cold Spring Harbor, N.Y.)2007
Histone modifications around individual BDNF gene promoters in prefrontal cortex are associated with extinction of conditioned fear.
Article in Learning & memory (Cold Spring Harbor, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 280 papers.
What it found
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Who cites it
280 citing papers in PubMed, 546 citations in OpenAlex.
- Trial
- Exercise Augmentation of Exposure Therapy for PTSD: Rationale and Pilot Efficacy Data.Cognitive behaviour therapy · 2015Trial
- The brain-derived neurotrophic factor Val66Met polymorphism predicts response to exposure therapy in posttraumatic stress disorder.Biological psychiatry · 2013Trial
- Epigenetic Mechanisms Underlying Cognitive Dysfunction in Parkinson's Disease: Current Evidence and Future Prospects.Brain and behavior · 2026Review
- Molecular architects of memory: BDNF/TrkB signaling and trafficking in neuronal plasticity and memory.Molecular psychiatry · 2026Review
- Aberrant Fear: Biological Underpinnings Relevant to Psychosis, Antipsychotic Drugs, and Psychotherapeutic Treatments, a Translational Approach.International journal of molecular sciences · 2026Review
- Multilayered regulation of BDNF DNA methylation in PTSD: a review from molecular mechanisms to trans generational inheritance.Frontiers in psychiatry · 2026Review
- HAT p300/CBP Activity in the Prelimbic Cortex Underlies Reconsolidation of Contextual Fear Memory.Molecular neurobiology · 2025Article
- Transcriptomic Architecture of Weak Versus Strong Contextual Fear Extinction Learning Uncovers Extinction-Suppressive Role of TIA1.Biological psychiatry global open science · 2025Article
- Sex-dependent role of hippocampal BDNF and GSK-3β in mediating PTSD-like behaviors in both sexes of adolescent rats exposed to fear conditioning, extinction, and reinstatement.Experimental brain research · 2025Article
- Polyphenol-Based Nutritional Strategies Combined With Exercise for Brain Function and Glioma Control: Focus on Epigenetic Modifications, Cognitive Function, Learning and Memory Processes.Food science & nutrition · 2025Review
- Brain-penetrant histone deacetylase inhibitor RG2833 improves spatial memory in females of an Alzheimer's disease rat model.Journal of Alzheimer's disease : JAD · 2025Article
- New Insights into Contradictory Changes in Brain-Derived Neurotrophic Factor (BDNF) in Rodent Models of Posttraumatic Stress Disorder (PTSD).Neurochemical research · 2024Review
- Involvement of dysregulated hippocampal histone H3K9 methylation at the promoter of the BDNF gene in impaired memory extinction.Psychopharmacology · 2024Article
- Transcriptome and acetylome profiling identify crucial steps of neuronal differentiation in Rubinstein-Taybi syndrome.Communications biology · 2024Article
- Ketamine's Amelioration of Fear Extinction in Adolescent Male Mice Is Associated with the Activation of the Hippocampal Akt-mTOR-GluA1 Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- DNA G-Quadruplex Is a Transcriptional Control Device That Regulates Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Unlocking the epigenetic symphony: histone acetylation's impact on neurobehavioral change in neurodegenerative disorders.Epigenomics · 2024Review
- Epigenetics of Fear, Anxiety and Stress - Focus on Histone Modifications.Current neuropharmacology · 2024Article
- Monoamine Oxidase: A Potential Link in Papez Circuit to Generalized Anxiety Disorders.CNS & neurological disorders drug targets · 2024Review
220 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extinction of conditioned fear is an important model both of inhibitory learning and of behavior therapy for human anxiety disorders. Like other forms of learning, extinction learning is long-lasting and depends on regulated gene expression. Epigenetic mechanisms make an important contribution to persistent changes in gene expression; therefore, in these studies, we have investigated whether epigenetic regulation of gene expression contributes to fear extinction. Since brain-derived neurotrophic factor (BDNF) is crucial for synaptic plasticity and for the maintenance of long-term memory, we examined histone modifications around two BDNF gene promoters after extinction of cued fear, as potential targets of learning-induced epigenetic regulation of gene expression. Valproic acid (VPA), used for some time as an anticonvulsant and a mood stabilizer, modulates the expression of BDNF, and is a histone deacetylase (HDAC) inhibitor. Here, we report that extinction of conditioned fear is accompanied by a significant increase in histone H4 acetylation around the BDNF P4 gene promoter and increases in BDNF exon I and IV mRNA expression in prefrontal cortex, that VPA enhances long-term memory for extinction because of its HDAC inhibitor effects, and that VPA potentiates the effect of weak extinction training on histone H4 acetylation around both the BDNF P1 and P4 gene promoters and on BDNF exon IV mRNA expression. These results suggest a relationship between histone H4 modification, epigenetic regulation of BDNF gene expression, and long-term memory for extinction of conditioned fear. In addition, they suggest that HDAC inhibitors may become a useful pharmacological adjunct to psychotherapy for human anxiety disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.