ArticleNature communications2025
Syngap1 promotes cognitive function through regulation of cortical sensorimotor dynamics.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Genetic Rescue of Disrupted Synaptic Protein Interaction Network Dynamics Following SYNGAP1 Reactivation.Molecular & cellular proteomics : MCP · 2026Article
- Translatable electrophysiological and behavioral abnormalities in a humanized model of SYNGAP1-disorder.Molecular psychiatry · 2026Article
- Syngap1 Synchronizes Relative Neuronal Maturation Across Cortical Areas to Organize Distributed Functional Networks.bioRxiv : the preprint server for biology · 2026Article
- The Endo-GeneScreen platform identifies drug-like probes that regulate endogenous protein levels within physiological contexts.Nature communications · 2025Article
- Genetic rescue of disrupted synaptic protein interaction network dynamics followingbioRxiv : the preprint server for biology · 2025Article
- AAV delivery of full-length SYNGAP1 rescues epileptic and behavioral phenotypes in a mouse model of SYNGAP1-related disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Dissecting mammalian cortical circuit development at single-cell resolution using inducible barcoded rabies virus.bioRxiv : the preprint server for biology · 2025Article
- CRISPR-mediated transcriptional activation as a mutation-independent therapeutic strategy forbioRxiv : the preprint server for biology · 2025Article
- Research progress inFrontiers in neurologyReview
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13 authors.
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Abstract
Perception, a cognitive construct, emerges through sensorimotor integration (SMI). The genetic mechanisms that shape SMI required for perception are unknown. Here, we demonstrate in mice that expression of the autism/intellectual disability gene, Syngap1, in cortical excitatory neurons is required for the formation of somatomotor networks that promote SMI-mediated perception. Cortical Syngap1 expression was necessary and sufficient for setting tactile sensitivity, sustaining tactile object exploration, and promoting tactile learning. Mice with deficient Syngap1 expression exhibited impaired neural dynamics induced by exploratory touches within a cortical-thalamic network that promotes attention and perception. Disrupted neuronal dynamics were associated with circuit-specific long-range synaptic connectivity abnormalities. Our data support a model where autonomous Syngap1 expression in cortical excitatory neurons promotes cognitive abilities through the assembly of long-range circuits that integrate temporally-overlapping sensory and motor signals, a process that promotes perception and attention. These data provide systems-level insights into the robust association between Syngap1 expression and cognitive ability.
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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.