ArticleNeurochemical research2016
Prenatal Exposure to Histone Deacetylase Inhibitors Affects Gene Expression of Autism-Related Molecules and Delays Neuronal Maturation.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Chrysin Ameliorates Valproic Acid Induced Autism Spectrum Behavioral Phenotypes Through Corticohippocampal Histone Deacetylase and Translational Modulation of SHANK3 Expression in Juvenile Rats.Journal of molecular neuroscience : MN · 2026Article
- Review
- Valproate-Induced Autism and Sexual Hormone Disturbances: A Literature Review and Hypotheses.Neurochemical research · 2025Review
- Reduced Neurite Arborization in Primary Dopaminergic Neurons in Autism-Like Shank3B-Deficient Mice.Molecular neurobiology · 2025Article
- Assessment of Expression of lncRNAs in Autistic Patients.Journal of molecular neuroscience : MN · 2024Article
- Three Decades of Valproate: A Current Model for Studying Autism Spectrum Disorder.Current neuropharmacology · 2024Review
- Modulation of human endogenous retroviruses and cytokines expression in peripheral blood mononuclear cells from autistic children and their parents.Retrovirology · 2022Article
- Phenotypic overlap between atopic dermatitis and autism.BMC neuroscience · 2021Article
- Enhanced drug delivery to the reproductive tract using nanomedicine reveals therapeutic options for prevention of preterm birth.Science translational medicine · 2021Article
- Alterations in the autonomic nerve activities of prenatal autism model mice treated with valproic acid at different developmental stages.Scientific reports · 2020Article
- Nuclear receptor corepressors in intellectual disability and autism.Molecular psychiatry · 2020Review
- Activation of the VPAC2 Receptor Impairs Axon Outgrowth and Decreases Dendritic Arborization in Mouse Cortical Neurons by a PKA-Dependent Mechanism.Frontiers in neuroscience · 2020Article
- Endogenous Retroviruses Activity as a Molecular Signature of Neurodevelopmental Disorders.International journal of molecular sciences · 2019Review
- Early Behavioral Alterations and Increased Expression of Endogenous Retroviruses Are Inherited Across Generations in Mice Prenatally Exposed to Valproic Acid.Molecular neurobiology · 2019Article
- Effects of rapamycin on social interaction deficits and gene expression in mice exposed to valproic acid in utero.Molecular brain · 2019Article
- Gut Microbiota and Fecal Metabolome Perturbation in Children with Autism Spectrum Disorder.Middle East journal of digestive diseases · 2018Review
- Aberrant Development and Synaptic Transmission of Cerebellar Cortex in a VPA Induced Mouse Autism Model.Frontiers in cellular neuroscience · 2018Article
- A Long-Term Treatment with Arachidonyl-2'-Chloroethylamide Combined with Valproate Increases Neurogenesis in a Mouse Pilocarpine Model of Epilepsy.International journal of molecular sciences · 2017Article
- Sexually Dimorphic Epigenetic Regulation of Brain-Derived Neurotrophic Factor in Fetal Brain in the Valproic Acid Model of Autism Spectrum Disorder.Developmental neuroscience · 2017Article
- Prenatal exposure to valproic acid increases miR-132 levels in the mouse embryonic brain.Molecular autism · 2017Article
Corrections and comments
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Authors and funding
10 authors.
Funding
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Abstract
Valproic acid (VPA) is a multi-target drug and an inhibitor of histone deacetylase (HDAC). We have previously demonstrated that prenatal exposure to VPA at embryonic day 12.5 (E12.5), but not at E14.5, causes autism-like behavioral abnormalities in male mouse offspring. We have also found that prenatal VPA exposure causes transient histone hyperacetylation in the embryonic brain, followed by decreased neuronal cell numbers in the prefrontal and somatosensory cortices after birth. In the present study, we examined whether prenatal HDAC inhibition affects neuronal maturation in primary mouse cortical neurons. Pregnant mice were injected intraperitoneally with VPA (500 mg/kg) and the more selective HDAC inhibitor trichostatin A (TSA; 500 µg/kg) at E12.5 or E14.5, and primary neuronal cultures were prepared from the cerebral cortices of their embryos. Prenatal exposure to VPA at E12.5, but not at E14.5, decreased total number, total length, and complexity of neuronal dendrites at 14 days in vitro (DIV). The effects of VPA weakened at 21 DIV. Exposure to TSA at E12.5, but not at E14.5, also delayed maturation of cortical neurons. In addition, real-time quantitative PCR revealed that the prenatal exposure to TSA decreased neuroligin-1 (Nlgn1), Shank2, and Shank3 mRNA levels and increased contactin-associated protein-like 2 mRNA level. The delay in neuronal maturation was also observed in Nlgn1-knockdown cells, which were transfected with Nlgn1 siRNA. These findings suggest that prenatal HDAC inhibition causes changes in gene expression of autism-related molecules linked to a delay of neuronal maturation.
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