ArticleeNeuro
Examining the Reversibility of Long-Term Behavioral Disruptions in Progeny of Maternal SSRI Exposure.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Chromosomal and gonadal sex have differing effects on social motivation in mice.Biology of sex differences · 2025Article
- Chromosomal and gonadal sex have differing effects on social motivation in mice.bioRxiv : the preprint server for biology · 2024Article
- Extensive characterization of a Williams syndrome murine model shows Gtf2ird1-mediated rescue of select sensorimotor tasks, but no effect on enhanced social behavior.Genes, brain, and behavior · 2023Article
- Extensive characterization of a Williams Syndrome murine model showsbioRxiv : the preprint server for biology · 2023Article
- Fluoxetine exposure throughout neurodevelopment differentially influences basilar dendritic morphology in the motor and prefrontal cortices.Scientific reports · 2022Article
- Influence of Prenatal Drug Exposure, Maternal Inflammation, and Parental Aging on the Development of Autism Spectrum Disorder.Frontiers in psychiatry · 2022Review
- Article
- Perinatal SSRI exposure affects brain functional activity associated with whisker stimulation in adolescent and adult rats.Scientific reports · 2021Article
- Ontogenetic Oxycodone Exposure Affects Early Life Communicative Behaviors, Sensorimotor Reflexes, and Weight Trajectory in Mice.Frontiers in behavioral neuroscience · 2021Article
- Gestational Factors throughout Fetal Neurodevelopment: The Serotonin Link.International journal of molecular sciences · 2020Review
- Functions of Gtf2i and Gtf2ird1 in the developing brain: transcription, DNA binding and long-term behavioral consequences.Human molecular genetics · 2020Article
- Studying the Contribution of Serotonin to Neurodevelopmental Disorders. Can This Fly?Frontiers in behavioral neuroscience · 2020Review
- Gtf2i and Gtf2ird1 mutation do not account for the full phenotypic effect of the Williams syndrome critical region in mouse models.Human molecular genetics · 2019Article
- Loss of CELF6 RNA binding protein impairs cocaine conditioned place preference and contextual fear conditioning.Genes, brain, and behavior · 2019Article
- Erroneous inference based on a lack of preference within one group: Autism, mice, and the social approach task.Autism research : official journal of the International Society for Autism Research · 2019Article
- Repeated neonatal isoflurane exposures in the mouse induce apoptotic degenerative changes in the brain and relatively mild long-term behavioral deficits.Scientific reports · 2019Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Serotonergic dysregulation is implicated in numerous psychiatric disorders. Serotonin plays widespread trophic roles during neurodevelopment; thus perturbations to this system during development may increase risk for neurodevelopmental disorders. Epidemiological studies have examined association between selective serotonin reuptake inhibitor (SSRI) treatment during pregnancy and increased autism spectrum disorder (ASD) risk in offspring. It is unclear from these studies whether ASD susceptibility is purely related to maternal psychiatric diagnosis, or if treatment poses additional risk. We sought to determine whether maternal SSRI treatment alone or in combination with genetically vulnerable background was sufficient to induce offspring behavior disruptions relevant to ASD. We exposed C57BL/6J or
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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.