ArticleNature2016
Thalamic reticular impairment underlies attention deficit in Ptchd1(Y/-) mice.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis 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
118 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.
- Analysing an allelic series of rare missense variants of CACNA1I in a Swedish schizophrenia cohort.Brain : a journal of neurology · 2022Pooled it
- Disruption of major Ptchd1 isoforms causes autistic traits in social behavior and communication.Molecular psychiatry · 2026Article
- Developmental Deficiency of Oligodendrocytes and Myelination in the Central Nervous System of the Fetal Alcohol Syndrome Mouse Model.CNS neuroscience & therapeutics · 2026Article
- Hyperactivation of distinct thalamic nuclei differentially impairs sleep physiology in rats.Molecular psychiatry · 2026Article
- Fever-like temperatures improve cognitive deficits in the Scn2a autism mouse model via increases in potassium channel activity.Molecular psychiatry · 2026Article
- Subcortical Dendritic Scaffolding in Autism Spectrum Disorder: A Testable ANK2-SCN2A-SHANK Framework.International journal of molecular sciences · 2026Review
- Article
- Electrical Coupling within Thalamocortical Networks Cumulatively Reduces Cortical Correlation to Sensory Inputs.eNeuro · 2026Article
- Reduced mediodorsal thalamus activity underlies aberrant belief dynamics in a genetic mouse model of schizophrenia.Nature neuroscience · 2026Article
- Resolving Diagnostic Uncertainty in Neurodevelopmental Disorders Using Exome Sequencing Supported by Literature-Based Multi-Omics Evidence.Biomolecules · 2026Article
- Rebound Bursting Selectively Enables Fast Dynamics in Dopamine Midbrain Neurons Projecting to the Dorsolateral Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- AAV-mediated peripheral scFv's administration to reduce cerebral tau in adult P301S transgenic mice: Mono-vs. combination therapy.Molecular therapy. Methods & clinical development · 2025Article
- Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism.Science advances · 2025Article
- Decoding gene networks controlling hypothalamic and prethalamic neuron development.Cell reports · 2025Article
- Decoding Gene Networks Controlling Hypothalamic and Prethalamic Neuron Development.bioRxiv : the preprint server for biology · 2025Article
- White-Matter Structural Connectivity and Alzheimer's Disease: A Mendelian Randomization Study.Brain and behavior · 2025Article
- Genetic variants in DDX53 contribute to autism spectrum disorder associated with the Xp22.11 locus.American journal of human genetics · 2025Article
- Distinct structural and functional connectivity of genetically segregated thalamoreticular subnetworks.Cell reports · 2024Article
- A prefrontal thalamocortical readout for conflict-related executive dysfunction in schizophrenia.Cell reports. Medicine · 2024Article
- Local activation of CB1 receptors by synthetic and endogenous cannabinoids dampens burst firing mode of reticular thalamic nucleus neurons in rats under ketamine anesthesia.Experimental brain research · 2024Article
58 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Developmental disabilities, including attention-deficit hyperactivity disorder (ADHD), intellectual disability (ID), and autism spectrum disorders (ASD), affect one in six children in the USA. Recently, gene mutations in patched domain containing 1 (PTCHD1) have been found in ~1% of patients with ID and ASD. Individuals with PTCHD1 deletion show symptoms of ADHD, sleep disruption, hypotonia, aggression, ASD, and ID. Although PTCHD1 is probably critical for normal development, the connection between its deletion and the ensuing behavioural defects is poorly understood. Here we report that during early post-natal development, mouse Ptchd1 is selectively expressed in the thalamic reticular nucleus (TRN), a group of GABAergic neurons that regulate thalamocortical transmission, sleep rhythms, and attention. Ptchd1 deletion attenuates TRN activity through mechanisms involving small conductance calcium-dependent potassium currents (SK). TRN-restricted deletion of Ptchd1 leads to attention deficits and hyperactivity, both of which are rescued by pharmacological augmentation of SK channel activity. Global Ptchd1 deletion recapitulates learning impairment, hyper-aggression, and motor defects, all of which are insensitive to SK pharmacological targeting and not found in the TRN-restricted deletion mouse. This study maps clinically relevant behavioural phenotypes onto TRN dysfunction in a human disease model, while also identifying molecular and circuit targets for intervention.
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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.