ArticleCell reports2018
SynDIG4/Prrt1 Is Required for Excitatory Synapse Development and Plasticity Underlying Cognitive Function.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Ternary Neurexin-T178-PTPR complexes represent a pre-synaptic core-module of neuronal synapse organization.Nature communications · 2026Article
- Article
- The AMPA receptor life cycle: assembly, regulation and synaptic diversity.Nature reviews. Neuroscience · 2026Review
- Native AMPA receptor architecture reveals SynDIG4 engagement and auxiliary subunit heterogeneity.Science advances · 2026Article
- Auxiliary subunits reshape structural asymmetry and functional plasticity in heterotetrameric GluA1/A2 AMPA receptor core.Nature communications · 2026Article
- Efficient and rapid isolation of native AMPA receptor complexes for cryo-EM.Protein science : a publication of the Protein Society · 2026Article
- 'Mini analysis' misrepresents changes in synaptic properties due to incomplete event detection.The Journal of physiology · 2025Article
- Multiscale proteomic modeling reveals protein networks driving Alzheimer's disease pathogenesis.Cell · 2025Article
- Regulation of hippocampal excitatory synapse development by the adhesion G-protein coupled receptor brain-specific angiogenesis inhibitor 2 (BAI2/ADGRB2).Molecular and cellular neurosciences · 2025Article
- Article
- Uncovering the epigenetic regulatory clues of PRRT1 in Alzheimer's disease: a strategy integrating multi-omics analysis with explainable machine learning.Alzheimer's research & therapy · 2025Article
- Epigenetics Modulators as Therapeutics for Neurological Disorders.Current pharmaceutical design · 2025Review
- AMPA receptors in the evolving synapse: structure, function, and disease implications.Frontiers in synaptic neuroscience · 2025Review
- Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling.Frontiers in pharmacology · 2025Article
- Dissecting the pathogenic effects of smoking in blood DNA methylation on allergic diseases.The World Allergy Organization journal · 2024Article
- Functional characterization of endocytic signals in the SynDIG/PRRT family members SynDIG1 and SynDIG4 in heterologous cells and neurons.Frontiers in cellular neuroscience · 2024Article
- Article
- A "multi-omics" analysis of blood-brain barrier and synaptic dysfunction in APOE4 mice.The Journal of experimental medicine · 2022Article
- The Role of AMPARs Composition and Trafficking in Synaptic Plasticity and Diseases.Cellular and molecular neurobiology · 2022Review
- Structural insights into function of ionotropic glutamate receptors.Biochemistry (Moscow) Supplement. Series A, Membrane and cell biology · 2022Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Altering AMPA receptor (AMPAR) content at synapses is a key mechanism underlying the regulation of synaptic strength during learning and memory. Previous work demonstrated that SynDIG1 (synapse differentiation-induced gene 1) encodes a transmembrane AMPAR-associated protein that regulates excitatory synapse strength and number. Here we show that the related protein SynDIG4 (also known as Prrt1) modifies AMPAR gating properties in a subunit-dependent manner. Young SynDIG4 knockout (KO) mice have weaker excitatory synapses, as evaluated by immunocytochemistry and electrophysiology. Adult SynDIG4 KO mice show complete loss of tetanus-induced long-term potentiation (LTP), while mEPSC amplitude is reduced by only 25%. Furthermore, SynDIG4 KO mice exhibit deficits in two independent cognitive assays. Given that SynDIG4 colocalizes with the AMPAR subunit GluA1 at non-synaptic sites, we propose that SynDIG4 maintains a pool of extrasynaptic AMPARs necessary for synapse development and function underlying higher-order cognitive plasticity.
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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.