ArticleJournal of neurophysiology2016
Morphine-induced synaptic plasticity in the VTA is reversed by HDAC inhibition.
Article in Journal of neurophysiology, 2016. 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, 34 citations in OpenAlex.
- Fentanyl Induces Behavioral Sensitization and Decreases Class IIa HDAC Expression-Activity in Brain as Measured by [Brain sciences · 2026Article
- The mechanism of the JNK signaling pathway in drug addiction : Author list.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Epigenetic Regulation of Inflammation by Dopamine in Primary Human Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic regulation of inflammation by dopamine in primary human macrophages.Frontiers in immunology · 2026Article
- Evaluation of AT121 versus morphine on cortical neurons electrophysiology and dopamine concentrations in hippocampal cells.PloS one · 2026Article
- LSD Restores Synaptic Plasticity in VTA of Morphine-Treated Mice and Disrupts Morphine-Conditioned Place Preference.bioRxiv : the preprint server for biology · 2025Article
- Sex differences in VTA GABA transmission and plasticity during opioid withdrawal.Scientific reports · 2023Article
- The role of the gut microbiome and microbial metabolism in mediating opioid-induced changes in the epigenome.Frontiers in microbiology · 2023Review
- Effects of prenatal opioid exposure on synaptic adaptations and behaviors across development.Neuropharmacology · 2023Review
- Addiction-induced plasticity in underlying neural circuits.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Chronic Δ9-tetrahydrocannabinol impact on plasticity, and differential activation requirement for CB1-dependent long-term depression in ventral tegmental area GABA neurons in adult versus young mice.Frontiers in neuroscience · 2022Article
- Drug addiction: from bench to bedside.Translational psychiatry · 2021Review
- Adolescent oxycodone exposure inhibits withdrawal-induced expression of genes associated with the dopamine transmission.Addiction biology · 2021Article
- Opioid-Induced Molecular and Cellular Plasticity of Ventral Tegmental Area Dopamine Neurons.Cold Spring Harbor perspectives in medicine · 2021Review
- Histone deacetylase inhibition reduces ventral tegmental area dopamine neuronal hyperexcitability involving AKAP150 signaling following maternal deprivation in juvenile male rats.Journal of neuroscience research · 2020Article
- Pharmacotherapeutic management of co-morbid alcohol and opioid use.Expert opinion on pharmacotherapy · 2020Review
- Early Life Stress- and Drug-Induced Histone Modifications Within the Ventral Tegmental Area.Frontiers in cell and developmental biology · 2020Review
- Histone Deacetylase Inhibitor Suberanilohydroxamic Acid Treatment Reverses Hyposensitivity to γ-Aminobutyric Acid in the Ventral Tegmental Area During Ethanol Withdrawal.Alcoholism, clinical and experimental research · 2018Article
- Targeting histone deacetylation for recovery of maternal deprivation-induced changes in BDNF and AKAP150 expression in the VTA.Experimental neurology · 2018Article
- Ethanol actions on the ventral tegmental area: novel potential targets on reward pathway neurons.Psychopharmacology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Dopamine (DA) dysfunction originating from the ventral tegmental area (VTA) occurs as a result of synaptic abnormalities following consumption of drugs of abuse and underlies behavioral plasticity associated with drug abuse. Drugs of abuse can cause changes in gene expression through epigenetic mechanisms in the brain that underlie some of the lasting neuroplasticity and behavior associated with addiction. Here we investigated the function of histone acetylation and histone deacetylase (HDAC)2 in the VTA in recovery of morphine-induced synaptic modifications following a single in vivo exposure to morphine. Using a combination of immunohistochemistry, Western blot, and whole cell patch-clamp recording in rat midbrain slices, we show that morphine increased HDAC2 activity in VTA DA neurons and reduced histone H3 acetylation at lysine 9 (Ac-H3K9) in the VTA 24 h after the injection. Morphine-induced synaptic changes at glutamatergic synapses involved endocannabinoid signaling to reduce GABAergic synaptic strength onto VTA DA neurons. Both plasticities were recovered by in vitro incubation of midbrain slices with a class I-specific HDAC inhibitor (HDACi), CI-994, through an increase in acetylation of histone H3K9. Interestingly, HDACi incubation also increased levels of Ac-H3K9 and triggered GABAergic and glutamatergic plasticities in DA neurons of saline-treated rats. Our results suggest that acute morphine-induced changes in VTA DA activity and synaptic transmission engage HDAC2 activity locally in the VTA to maintain synaptic modifications through histone hypoacetylation.
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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.