ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Synaptic and intrinsic balancing during postnatal development in rat pups exposed to valproic acid in utero.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Gestational valproic acid exposure enhances facial stimulation-evoked cerebellar mossy fiber-granule cell transmission via GluN2A subunit-containing NMDA receptor in offspring mice.Translational psychiatry · 2024Article
- The protective role of prenatal administration of ascorbic acid on autistic-like behavior in a rat model of autism.IBRO neuroscience reports · 2024Article
- Group I and group II metabotropic glutamate receptors are upregulated in the synapses of infant rats prenatally exposed to valproic acid.Psychopharmacology · 2023Article
- Creation of Neuronal Ensembles and Cell-Specific Homeostatic Plasticity through Chronic Sparse Optogenetic Stimulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- The Role of Zinc and NMDA Receptors in Autism Spectrum Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Assessment of behavioral, morphological and electrophysiological changes in prenatal and postnatal valproate induced rat models of autism spectrum disorder.Scientific reports · 2021Article
- Long-Lasting Changes in Glial Cells Isolated From Rats Subjected to the Valproic Acid Model of Autism Spectrum Disorder.Frontiers in pharmacology · 2021Article
- Consequences of prenatal exposure to valproic acid in the socially monogamous prairie voles.Scientific reports · 2019Article
- Pathway-Specific Drive of Cerebellar Golgi Cells Reveals Integrative Rules of Cortical Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Molecular Pathology and Pharmacological Treatment of Autism Spectrum Disorder-Like Phenotypes Using Rodent Models.Frontiers in cellular neuroscience · 2018Review
- Distinct Defects in Synaptic Differentiation of Neocortical Neurons in Response to Prenatal Valproate Exposure.Scientific reports · 2016Article
- Clinical and Neurobiological Relevance of Current Animal Models of Autism Spectrum Disorders.Biomolecules & therapeutics · 2016Review
- Prenatal Valproate Exposure Differentially Affects Parvalbumin-Expressing Neurons and Related Circuits in the Cortex and Striatum of Mice.Frontiers in molecular neuroscience · 2016Article
- MeCP2 Modulates Sex Differences in the Postsynaptic Development of the Valproate Animal Model of Autism.Molecular neurobiology · 2016Article
- Valproate-induced neurodevelopmental deficits in Xenopus laevis tadpoles.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Impaired Processing in the Primary Auditory Cortex of an Animal Model of Autism.Frontiers in systems neuroscience · 2015Article
- Predictable enriched environment prevents development of hyper-emotionality in the VPA rat model of autism.Frontiers in neuroscience · 2015Article
- Suppression of NMDA receptor function in mice prenatally exposed to valproic acid improves social deficits and repetitive behaviors.Frontiers in molecular neuroscience · 2015Article
- Late onset deficits in synaptic plasticity in the valproic acid rat model of autism.Frontiers in cellular neuroscience · 2014Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Valproic acid (VPA) is among the most teratogenic of commonly prescribed anticonvulsants, increasing the risk in humans of major malformations and impaired cognitive development. Likewise, rats exposed prenatally to VPA exhibit a variety of neuroanatomical and behavioral abnormalities. Previous work has shown that pyramidal neuron physiology in young VPA-exposed animals is marked by two strong abnormalities: an impairment in intrinsic neuronal excitability and an increase in NMDA synaptic currents. In this study, we investigated these abnormalities across postnatal development using whole-cell patch recordings from layer 2/3 neurons of medial prefrontal cortex. We found that both abnormalities were at a peak soon after birth but were gradually corrected as animals matured, to the extent that normal excitability and NMDA currents had been restored by early adolescence. The manner in which this correction happened suggested coordination between the two processes. Using computational models fitted to the physiological data, we argue that the two abnormalities trade off against each other, with the effects on network activity of the one balancing the effects of the other. This may constitute part of the nervous system's homeostatic response to teratogenic insult: an attempt to maintain stability despite a strong challenge.
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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.