ArticleCerebral cortex (New York, N.Y. : 1991)2018
Mouse Cntnap2 and Human CNTNAP2 ASD Alleles Cell Autonomously Regulate PV+ Cortical Interneurons.
Article in Cerebral cortex (New York, N.Y. : 1991), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 104 citations in OpenAlex.
- Complementary vertebrateeLife · 2026Article
- Autism-like behavior induced by conditional ablation of the Bassoon gene in GABAergic interneurons.Molecular psychiatry · 2026Article
- Lower Striatal and Cortical Calretinin Interneuron Density Associated With Altered Social Behavior in Cntnap2 Knockout Mice.Autism research : official journal of the International Society for Autism Research · 2026Article
- <p>Harnessing MSC‑derived exosomes to modulate the pathophysiology of ASD: Recent advances and therapeutic implications (Review)</p>.International journal of molecular medicine · 2026Review
- In utero exposure to anti-Caspr2 antibody disrupts parvalbumin interneuron function in the hippocampus.Brain, behavior, and immunity · 2026Article
- CASPR2 Autoimmune Antibodies Induce Neuronal Hyperactivity in Human Brain Organoids.Journal of neurochemistry · 2026Article
- CNTNAP2: isoform- and context-specific functions in neurological disorders and cancer.Frontiers in cellular neuroscience · 2026Review
- Shared Disease Mechanisms in Neurodevelopmental Disorders: A Cellular and Molecular Biology Perspective.Brain sciences · 2025Review
- Early postnatal dysfunction of ACC PV interneurons in Shank3BMolecular psychiatry · 2025Article
- A postnatal molecular switch drives activity-dependent maturation of parvalbumin interneurons.Cell · 2025Article
- Complimentary vertebratebioRxiv : the preprint server for biology · 2025Article
- Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism.Science advances · 2025Article
- Genetic Signatures of Competitive Performance in Burmese Gamecocks: A Transcriptomic Analysis.Biology · 2025Article
- Kazakh Tobet dogs in the genomic landscape: refining the history of livestock guardian breeds.BMC biology · 2025Article
- Article
- Interneuron Diversity: How Form Becomes Function.Cold Spring Harbor perspectives in biology · 2025Review
- Degraded tactile coding in the Cntnap2 mouse model of autism.Cell reports · 2024Article
- Maternal immunoglobulin G affects brain development of mouse offspring.Journal of neuroinflammation · 2024Article
- Neuroanatomical Alterations in the CNTNAP2 Mouse Model of Autism Spectrum Disorder.Brain sciences · 2023Article
- Developmental changes in electrophysiological properties of auditory cortical neurons in theJournal of neurophysiology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Human mutations in CNTNAP2 are associated with an array of neuropsychiatric and neurological syndromes, including speech and language disorders, epilepsy, and autism spectrum disorder (ASD). We examined Cntnap2's expression and function in GABAergic cortical interneurons (CINs), where its RNA is present at highest levels in chandelier neurons, PV+ neurons and VIP+ neurons. In vivo functions were studied using both constitutive Cntnap2 null mice and a transplantation assay, the latter to assess cell autonomous phenotypes of medial ganglionic eminence (MGE)-derived CINs. We found that Cntnap2 constitutive null mutants had normal numbers of MGE-derived CINs, but had reduced PV+ CINs. Transplantation assays showed that Cntnap2 cell autonomously regulated the physiology of parvalbumin (PV)+, fast-spiking CINs; no phenotypes were observed in somatostatin+, regular spiking, CINs. We also tested the effects of 4 human CNTNAP2 ASD missense mutations in vivo, and found that they impaired PV+ CIN development. Together, these data reveal that reduced CNTNAP2 function impairs PV+ CINs, a cell type with important roles in regulating cortical circuits.
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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.