ReviewProgress in neuro-psychopharmacology & biological psychiatry2015
NMDA receptor activation regulates sociability by its effect on mTOR signaling activity.
Review in Progress in neuro-psychopharmacology & biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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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
27 citing papers in PubMed, 55 citations in OpenAlex.
- Inactivation of NMDAR and CaMKII signaling within the prelimbic cortex blocks incubated cocaine- and sucrose-craving.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Promotion of lung cancer growth via glutamate ionotropic receptor N-methyl-D-aspartate-type subunit 2D (Journal of thoracic disease · 2026Article
- Emerging Epigenetic Therapeutics and Diagnostics for Autism Spectrum Disorder.Current issues in molecular biology · 2025Review
- Differential regulation of mTOR activity in retinal ganglion cells underlies their distinct susceptibility to ischemia/reperfusion.Communications biology · 2025Article
- An elderly case of paraneoplastic anti-NMDA receptor encephalitis associated with large cell neuroendocrine carcinoma of the lung.BMC pulmonary medicine · 2024Article
- Effects of hyperbaric oxygen therapy on autistic behaviors andFrontiers in neuroscience · 2024Article
- Proteomic association with age-dependent sex differences in Wisconsin Card Sorting Test performance in healthy Thai subjects.Scientific reports · 2023Article
- Sex and age differences in social and cognitive function in offspring exposed to late gestational hypoxia.Biology of sex differences · 2023Article
- Stimulation of synaptic activity promotes TFEB-mediated clearance of pathological MAPT/Tau in cellular and mouse models of tauopathies.Autophagy · 2023Article
- Possible role of NO/NMDA pathway in the autistic-like behaviors induced by maternal separation stress in mice.PloS one · 2023Article
- Roles and Mechanisms of Astragaloside IV in Combating Neuronal Aging.Aging and disease · 2022Review
- Single cell transcriptomics reveals dysregulated cellular and molecular networks in a fragile X syndrome model.PLoS genetics · 2022Article
- GluN2A-ERK-mTOR pathway confers a vulnerability to LPS-induced depressive-like behaviour.Behavioural brain research · 2022Article
- Review
- Nutritional Support of Neurodevelopment and Cognitive Function in Infants and Young Children-An Update and Novel Insights.Nutrients · 2021Review
- From Hyposociability to Hypersociability-The Effects of PSD-95 Deficiency on the Dysfunctional Development of Social Behavior.Frontiers in behavioral neuroscience · 2021Article
- Recapitulation of Neuropsychiatric Behavioral Features in Mice Using Acute Low-dose MK-801 Administration.Experimental neurobiology · 2019Article
- Glutamate in cancers: from metabolism to signaling.Journal of biomedical research · 2019Article
- Crosstalk Between Inflammation and Glutamate System in Depression: Signaling Pathway and Molecular Biomarkers for Ketamine's Antidepressant Effect.Molecular neurobiology · 2019Review
- Sex Differences in Autism Spectrum Disorder: a Review.Current psychiatry reports · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tuberous Sclerosis Complex is one example of a syndromic form of autism spectrum disorder associated with disinhibited activity of mTORC1 in neurons (e.g., cerebellar Purkinje cells). mTORC1 is a complex protein possessing serine/threonine kinase activity and a key downstream molecule in a signaling cascade beginning at the cell surface with the transduction of neurotransmitters (e.g., glutamate and acetylcholine) and nerve growth factors (e.g., Brain-Derived Neurotrophic Factor). Interestingly, the severity of the intellectual disability in Tuberous Sclerosis Complex may relate more to this metabolic disturbance (i.e., overactivity of mTOR signaling) than the density of cortical tubers. Several recent reports showed that rapamycin, an inhibitor of mTORC1, improved sociability and other symptoms in mouse models of Tuberous Sclerosis Complex and autism spectrum disorder, consistent with mTORC1 overactivity playing an important pathogenic role. NMDA receptor activation may also dampen mTORC1 activity by at least two possible mechanisms: regulating intraneuronal accumulation of arginine and the phosphorylation status of a specific extracellular signal regulating kinase (i.e., ERK1/2), both of which are "drivers" of mTORC1 activity. Conceivably, the prosocial effects of targeting the NMDA receptor with agonists in mouse models of autism spectrum disorders result from their ability to dampen mTORC1 activity in neurons. Strategies for dampening mTORC1 overactivity by NMDA receptor activation may be preferred to its direct inhibition in chronic neurodevelopmental disorders, such as autism spectrum disorders.
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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.