ArticleThe international journal of neuropsychopharmacology2018
Involvement of Epigenetic Modifications of GABAergic Interneurons in Basolateral Amygdala in Anxiety-like Phenotype of Prenatally Stressed Mice.
Article in The international journal of neuropsychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- DNMT1-mediated central amygdala to locus coeruleus circuit contributes to chronic pain-related depression in mice.Acta pharmacologica Sinica · 2026Article
- A Dnmt3a-Mediated Epigenetic Mechanism for Chronic-Pain-Induced Behaviors of Negative Emotion in Mice.Cells · 2026Article
- The impact of pregestational stress on neurodevelopment: Implications for autism spectrum disorder and attention-deficit/hyperactivity disorder.The Journal of physiology · 2026Review
- Serotonin receptor 4 in the ventral CA3 regulates agomelatine-induced anxiolytic-like behaviors.Acta pharmacologica Sinica · 2026Article
- Role of LncRNA in Trauma Susceptibility and Resilience to Post-Traumatic Stress Disorder (PTSD): A Pilot Study in the African American Population.Neuropsychiatric disease and treatment · 2025Article
- The role of epigenetics in anxiety disorders.Molecular biology reports · 2023Review
- Does Morphine Exposure Before Gestation Change Anxiety-Like Behavior During Morphine Dependence in Male Wistar Rats?Addiction & health · 2023Article
- The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review.eNeuro · 2023Review
- Exposure to Juvenile Stress Induces Epigenetic Alterations in the GABAergic System in Rats.Genes · 2023Article
- Impact of stress on inhibitory neuronal circuits, our tribute to Bruce McEwen.Neurobiology of stress · 2022Article
- Apocynin Prevents Anxiety-Like Behavior and Histone Deacetylases Overexpression Induced by Sub-Chronic Stress in Mice.Biomolecules · 2021Article
- Causal roles of stress kinase JNK2 in DNA methylation and binge alcohol withdrawal-evoked behavioral deficits.Pharmacological research · 2021Article
- The Potential Role of Epigenetic Drugs in the Treatment of Anxiety Disorders.Neuropsychiatric disease and treatment · 2020Review
- Enrichment of Genomic Pathways Based on Differential DNA Methylation Associated With Chronic Postsurgical Pain and Anxiety in Children: A Prospective, Pilot Study.The journal of pain · 2019Observational
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Prenatal stress is considered a risk factor for anxiety disorder. Downregulation in the expression of GABAergic gene, that is, glutamic acid decarboxylase 67, associated with DNA methyltransferase overexpression in GABAergic neurons has been regarded as a characteristic component of anxiety disorder. Prenatal stress has an adverse effect on the development of the basolateral amygdala, which is a key region in anxiety regulation. The aim of this study is to analyze the possibility of epigenetic alterations of GABAergic neurons in the basolateral amygdala participating in prenatal stress-induced anxiety. Methods: Behavioral tests were used to explore the prenatal stress-induced anxiety behaviors of female adult mice. Real-time RT-PCR, western blot, chromatin immunoprecipitation, and electrophysiological analysis were employed to detect epigenetic changes of GABAergic system in the basolateral amygdala. Results: Prenatal stress mice developed an anxiety-like phenotype accompanied by a significant increase of DNA methyltransferase 1 and a reduced expression of glutamic acid decarboxylase 67 in the basolateral amygdala. Prenatal stress mice also showed the increased binding of DNA methyltransferase 1 and methyl CpG binding protein 2 to glutamic acid decarboxylase 67 promoter region. The decrease of glutamic acid decarboxylase 67 transcript was paralleled by an enrichment of 5-methylcytosine in glutamic acid decarboxylase 67 promoter regions. Electrophysiological study revealed the increase of postsynaptic neuronal excitability in the cortical-basolateral amygdala synaptic transmission of prenatal stress mice. 5-Aza-deoxycytidine treatment restored the increased synaptic transmission and anxiety-like behaviors in prenatal stress mice via improving GABAergic system. Conclusion: The above results suggest that DNA epigenetic modifications of GABAergic interneurons in the basolateral amygdala participate in the etiology of anxiety-like phenotype in prenatal stress mice.
Indexed as
Identifiers
What OpenQuestion holds
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.