ArticleProceedings of the National Academy of Sciences of the United States of America2015
Synaptic abnormalities and cytoplasmic glutamate receptor aggregates in contactin associated protein-like 2/Caspr2 knockout neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.
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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
86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 142 citations in OpenAlex.
- Retrograde Amnesia in LGI1 and CASPR2 Limbic Encephalitis: Two Case Reports and a Systematic Literature Review.European journal of neurology · 2025Pooled it
- Endosomal system genetics and autism spectrum disorders: A literature review.Neuroscience and biobehavioral reviews · 2016Pooled it
- Nematode extracellular protein interactome expands connections between signaling pathways.Cell genomics · 2026Article
- Spatial multiomics dissects the SARS-CoV-2-induced disruption of cell adhesion and immune dynamics in the human hippocampus.Journal of neuroinflammation · 2026Article
- CASPR2 Autoimmune Antibodies Induce Neuronal Hyperactivity in Human Brain Organoids.Journal of neurochemistry · 2026Article
- Third-generation whole-genome sequencing reveals the role of CNTNAP2 as a tumor suppressor gene in high-risk neuroblastomas.Journal of translational medicine · 2026Article
- CNTNAP2: isoform- and context-specific functions in neurological disorders and cancer.Frontiers in cellular neuroscience · 2026Review
- Heterogeneity of anti-Caspr2 antibodies: specificity and pathogenicity.Translational psychiatry · 2025Article
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
- Article
- Age-Dependent Effects of Loss of Contactin-Associated Protein-Like 2, an Autism-Associated Gene, on the Acquisition and Recall of Fear Memory.Autism research : official journal of the International Society for Autism Research · 2025Article
- Postnatal environment affects auditory development and sensorimotor gating in a rat model for autism spectrum disorder.Frontiers in neuroscience · 2025Article
- Transient CSF1R inhibition ameliorates behavioral deficits in Cntnap2 knockout and valproic acid-exposed mouse models of autism.Journal of neuroinflammation · 2024Article
- nlr-1/CNTNAP regulates dopamine circuit structure and foraging behaviors in C. elegans.Communications biology · 2024Article
- Nematode Extracellular Protein Interactome Expands Connections between Signaling Pathways.bioRxiv : the preprint server for biology · 2024Article
- Etiologies underlying sex bias in autism spectrum disorder: a narrative review of preclinical rodent models.Ewha medical journal · 2024Review
- Contactin-associated protein-like 2 (CNTNAP2) mutations impair the essential α-secretase cleavages, leading to autism-like phenotypes.Signal transduction and targeted therapy · 2024Article
- Low Plasma Levels of Contactin-Associated Protein-Like 2 in Children with Autism Spectrum Disorder: Links to Neural Development.Neuropsychiatric disease and treatment · 2024Article
- Assessing the Cntnap2 knockout rat prepulse inhibition deficit through prepulse scaling of the baseline startle response curve.Translational psychiatry · 2023Article
- Molecular Mechanisms Underlying NMDARs Dysfunction and Their Role in ADHD Pathogenesis.International journal of molecular sciences · 2023Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Central glutamatergic synapses and the molecular pathways that control them are emerging as common substrates in the pathogenesis of mental disorders. Genetic variation in the contactin associated protein-like 2 (CNTNAP2) gene, including copy number variations, exon deletions, truncations, single nucleotide variants, and polymorphisms have been associated with intellectual disability, epilepsy, schizophrenia, language disorders, and autism. CNTNAP2, encoded by Cntnap2, is required for dendritic spine development and its absence causes disease-related phenotypes in mice. However, the mechanisms whereby CNTNAP2 regulates glutamatergic synapses are not known, and cellular phenotypes have not been investigated in Cntnap2 knockout neurons. Here we show that CNTNAP2 is present in dendritic spines, as well as axons and soma. Structured illumination superresolution microscopy reveals closer proximity to excitatory, rather than inhibitory synaptic markers. CNTNAP2 does not promote the formation of synapses and cultured neurons from Cntnap2 knockout mice do not show early defects in axon and dendrite outgrowth, suggesting that CNTNAP2 is not required at this stage. However, mature neurons from knockout mice show reduced spine density and levels of GluA1 subunits of AMPA receptors in spines. Unexpectedly, knockout neurons show large cytoplasmic aggregates of GluA1. Here we characterize, for the first time to our knowledge, synaptic phenotypes in Cntnap2 knockout neurons and reveal a novel role for CNTNAP2 in GluA1 trafficking. Taken together, our findings provide insight into the biological roles of CNTNAP2 and into the pathogenesis of CNTNAP2-associated neuropsychiatric 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.