ArticleBrain research bulletin2014
Rapamycin improves sociability in the BTBR T(+)Itpr3(tf)/J mouse model of autism spectrum disorders.
Article in Brain research bulletin, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 66 citations in OpenAlex.
- Acute rapamycin treatment reveals distinct mechanisms of dysfunction in a maternal inflammation mouse model.Nature communications · 2026Article
- The identification of metabolites from gut microbiota in autism spectrum disorder via network pharmacology.Scientific reports · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Biomimetic nanoparticles with enhanced rapamycin delivery for autism spectrum disorder treatment via autophagy activation and oxidative stress modulation.Theranostics · 2024Article
- UBE3A: The Role in Autism Spectrum Disorders (ASDs) and a Potential Candidate for Biomarker Studies and Designing Therapeutic Strategies.Diseases (Basel, Switzerland) · 2023Review
- Maturation of nucleus accumbens synaptic transmission signals a critical period for the rescue of social deficits in a mouse model of autism spectrum disorder.Molecular brain · 2023Article
- mTOR pathway - a potential therapeutic target in stroke.Therapeutic advances in neurological disorders · 2023Review
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- From bench to bedside: The mGluR5 system in people with and without Autism Spectrum Disorder and animal model systems.Translational psychiatry · 2022Article
- The trilateral interactions between mammalian target of rapamycin (mTOR) signaling, the circadian clock, and psychiatric disorders: an emerging model.Translational psychiatry · 2022Review
- Review
- Altered nociceptive behavior and emotional contagion of pain in mouse models of autism.Genes, brain, and behavior · 2022Article
- Repetitive Restricted Behaviors in Autism Spectrum Disorder: From Mechanism to Development of Therapeutics.Frontiers in neuroscience · 2022Review
- The HECT E3 Ligase E6AP/UBE3A as a Therapeutic Target in Cancer and Neurological Disorders.Cancers · 2020Review
- Intergenerational Metabolic Syndrome and Neuronal Network Hyperexcitability in Autism.Trends in neurosciences · 2019Review
- Hypothesis-driven investigations of diverse pharmacological targets in two mouse models of autism.Autism research : official journal of the International Society for Autism Research · 2019Article
- Suppression of Akt-mTOR pathway rescued the social behavior in Cntnap2-deficient mice.Scientific reports · 2019Article
- The Gut-Immune-Brain Axis in Autism Spectrum Disorders; A Focus on Amino Acids.Frontiers in endocrinology · 2019Review
- Insulin-Like Growth Factor II Targets the mTOR Pathway to Reverse Autism-Like Phenotypes in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Overactivation of the mammalian target of rapamycin (mTOR) has been implicated in the pathogenesis of syndromic forms of autism spectrum disorders (ASDs), such as tuberous sclerosis complex, neurofibromatosis 1, and fragile X syndrome. Administration of mTORC1 (mTOR complex 1) inhibitors (e.g. rapamycin) in syndromic mouse models of ASDs improved behavior, cognition, and neuropathology. However, since only a minority of ASDs are due to the effects of single genes (∼10%), there is a need to explore inhibition of mTOR activity in mouse models that may be more relevant to the majority of nonsyndromic presentations, such as the genetically inbred BTBR T(+)Itpr3(tf)/J (BTBR) mouse model of ASDs. BTBR mice have social impairment and exhibit increased stereotypic behavior. In prior work, d-cycloserine, a partial glycineB site agonist that targets the N-methyl-d-aspartate (NMDA) receptor, was shown to improve sociability in both Balb/c and BTBR mouse models of ASDs. Importantly, NMDA receptor activation regulates mTOR signaling activity. The current study investigated the ability of rapamycin (10mg/kg, i.p.×four days), an mTORC1 inhibitor, to improve sociability and stereotypic behavior in BTBR mice. Using a standard paradigm to assess mouse social behavior, rapamycin improved several measures of sociability in the BTBR mouse, suggesting that mTOR overactivation represents a therapeutic target that mediates or contributes to impaired sociability in the BTBR mouse model of ASDs. Interestingly, there was no effect of rapamycin on stereotypic behaviors in this mouse model.
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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.