ArticleCerebral cortex (New York, N.Y. : 1991)2017
Pharmacological Modulation of AMPAR Rescues Intellectual Disability-Like Phenotype in Tm4sf2-/y Mice.
Article in Cerebral cortex (New York, N.Y. : 1991), 2017. 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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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Positive AMPA and Kainate Receptor Modulators and Their Therapeutic Potential in CNS Diseases: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Tetraspanin7 in adipose tissue remodeling and its impact on metabolic health.Molecular metabolism · 2025Article
- New insights into the role of tetraspanin 6, 7, and 8 in physiology and pathology.Cancer medicine · 2024Review
- Neuronal network activity and connectivity are impaired in a conditional knockout mouse model with PCDH19 mosaic expression.Molecular psychiatry · 2024Article
- The role of Tetraspanins in digestive system tumor development: update and emerging evidence.Frontiers in cell and developmental biology · 2024Review
- Enhanced Activation of the S1PR2-IL-1β-Src-BDNF-TrkB Pathway Mediates Neuroinflammation in the Hippocampus and Cognitive Impairment in Hyperammonemic Rats.International journal of molecular sciences · 2023Article
- The Labyrinthine Landscape of APP Processing: State of the Art and Possible Novel Soluble APP-Related Molecular Players in Traumatic Brain Injury and Neurodegeneration.International journal of molecular sciences · 2023Article
- Integrin β1/FAK/SRC signal pathway is involved in autism spectrum disorder inLife science alliance · 2023Article
- Article
- Exploiting volume electron microscopy to investigate structural plasticity and stability of the postsynaptic compartment of central synapses.Frontiers in cellular neuroscience · 2023Review
- Diversity of AMPA Receptor Ligands: Chemotypes, Binding Modes, Mechanisms of Action, and Therapeutic Effects.Biomolecules · 2022Review
- Loss of tetraspanin-7 expression reduces pancreatic β-cell exocytosis CaDiabetic medicine : a journal of the British Diabetic Association · 2022Article
- ATM rules neurodevelopment and glutamatergic transmission in the hippocampus but not in the cortex.Cell death & disease · 2022Article
- Positive AMPA receptor modulation in the treatment of neuropsychiatric disorders: A long and winding road.Drug discovery today · 2021Review
- Arhgap22 Disruption Leads to RAC1 Hyperactivity Affecting Hippocampal Glutamatergic Synapses and Cognition in Mice.Molecular neurobiology · 2021Article
- RAB39B-mediated trafficking of the GluA2-AMPAR subunit controls dendritic spine maturation and intellectual disability-related behaviour.Molecular psychiatry · 2021Article
- Microglial vesicles improve post-stroke recovery by preventing immune cell senescence and favoring oligodendrogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- A mouse model of Bardet-Biedl Syndrome has impaired fear memory, which is rescued by lithium treatment.PLoS genetics · 2021Article
- The DNA repair protein ATM as a target in autism spectrum disorder.JCI insight · 2021Article
- Modeling suggests combined-drug treatments for disorders impairing synaptic plasticity via shared signaling pathways.Journal of computational neuroscience · 2021Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intellectual disability affects 2-3% of the world's population and typically begins during childhood, causing impairments in social skills and cognitive abilities. Mutations in the TM4SF2 gene, which encodes the TSPAN7 protein, cause a severe form of intellectual disability, and currently, no therapy is able to ameliorate this cognitive impairment. We previously reported that, in cultured neurons, shRNA-mediated down-regulation of TSPAN7 affects AMPAR trafficking by enhancing PICK1-GluA2 interaction, thereby increasing the intracellular retention of AMPAR. Here, we found that loss of TSPAN7 function in mice causes alterations in hippocampal excitatory synapse structure and functionality as well as cognitive impairment. These changes occurred along with alterations in AMPAR expression levels. We also found that interfering with PICK1-GluA2 binding restored synaptic function in Tm4sf2-/y mice. Moreover, potentiation of AMPAR activity via the administration of the ampakine CX516 reverted the neurological phenotype observed in Tm4sf2-/y mice, suggesting that pharmacological modulation of AMPAR may represent a new approach for treating patients affected by TM4SF2 mutations and intellectual disability.
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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.