ArticleMolecular autism2017
Effects of a social stimulus on gene expression in a mouse model of fragile X syndrome.
Article in Molecular autism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Therapeutic efficacy of the BKCa channel opener chlorzoxazone in a mouse model of Fragile X syndrome.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Altered projection-specific synaptic remodeling and its modification by oxytocin in an idiopathic autism marmoset model.Communications biology · 2024Article
- Neuronal Ensembles in the Amygdala Allow Social Information to Motivate Later Decisions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Distinct dynamics of social motivation drive differential social behavior in laboratory rat and mouse strains.Nature communications · 2020Article
- A social encounter drives gene expression changes linked to neuronal function, brain development, and related disorders in mice expressing the serotonin transporter Ala56 variant.Neuroscience letters · 2020Article
- (ACS pharmacology & translational science · 2020Article
- Convergence of spectrums: neuronal gene network states in autism spectrum disorder.Current opinion in neurobiology · 2019Review
- Chronic restraint stress impairs sociability but not social recognition and spatial memoryin C57BL/6J mice.Experimental animals · 2019Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundPeople with fragile X syndrome (FXS) often have deficits in social behavior, and a substantial portion meet criteria for autism spectrum disorder. Though the genetic cause of FXS is known to be due to the silencing of
methods
resultsImmunohistochemistry revealed a significantly greater number of c-Fos-positive cells in the lateral amygdala and medial amygdala in the brains of mice exposed to a social stimulus, compared to a non-social stimulus. In the prelimbic cortex, there was no significant effect of social stimulus; although the number of c-Fos-positive cells was lower in the social condition compared to the non-social condition, and negatively correlated with c-Fos in the amygdala. RNA sequencing revealed differentially expressed genes enriched for molecules known to interact with FMRP and also for autism-related genes identified in the Simons Foundation Autism Research Initiative gene database. Ingenuity Pathway Analysis detected enrichment of differentially expressed genes in networks and pathways related to neuronal development, intracellular signaling, and inflammatory response.
conclusionsUsing the
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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.