ArticleNature communications2020
Hyperactivated PTP1B phosphatase in parvalbumin neurons alters anterior cingulate inhibitory circuits and induces autism-like behaviors.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Systematic review and meta-analysis: multimodal functional and anatomical neural alterations in autism spectrum disorder.Molecular autism · 2024Pooled it
- Enhanced expression of spinal PTP1B contributes to peripheral inflammation- induced glycinergic disinhibition and mechanical pain.Communications biology · 2026Article
- PTP1B in astrocytes drives pathogen-induced neurodegeneration.Journal of neuroinflammation · 2026Article
- A distinct lineage pathway drives parvalbumin chandelier cell fate in human interneuron reprogramming.Science advances · 2026Article
- Subtype-Specific Roles of Anterior Cingulate Cortex Neurons in Pain-Induced Social Deficits in Mice.Theranostics · 2026Article
- Early postnatal dysfunction of ACC PV interneurons in Shank3BMolecular psychiatry · 2025Article
- Differential brain activation and network connectivity in social interactions presence and absence of physical contact.Communications biology · 2025Article
- Upregulated inwardly rectifying KJournal of biomedical research · 2025Article
- A Systems Biology Approach for Prioritizing ASD Genes in Large or Noisy Datasets.International journal of molecular sciences · 2025Article
- The Balance in the Head: How Developmental Factors Explain Relationships Between Brain Asymmetries and Mental Diseases.Brain sciences · 2025Review
- Immediate and sustained effects of acupuncture on the default mode network.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2025Article
- Discovering functional interactions among schizophrenia-risk genes by combining behavioral genetics with cell biology.Neuroscience and biobehavioral reviews · 2024Review
- Deconstruction the feedforward inhibition changes in the layer III of anterior cingulate cortex after peripheral nerve injury.Communications biology · 2024Article
- PV and SST neurons in the anterior cingulate cortex regulate social disorders in adulthood induced by sensory abnormalities in childhood.CNS neuroscience & therapeutics · 2024Article
- SARM1 deletion in parvalbumin neurons is associated with autism-like behaviors in mice.Cell death & disease · 2022Article
- Development, Diversity, and Death of MGE-Derived Cortical Interneurons.International journal of molecular sciences · 2021Review
- Conditional Pten knockout in parvalbumin- or somatostatin-positive neurons sufficiently leads to autism-related behavioral phenotypes.Molecular brain · 2021Article
- Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models.Neural regeneration research · 2021Article
- Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm.Molecular autism · 2020Article
- Activation of tyrosine phosphatases in the progression of Alzheimer's disease.Neural regeneration research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Individuals with autism spectrum disorder (ASD) have social interaction deficits and difficulty filtering information. Inhibitory interneurons filter information at pyramidal neurons of the anterior cingulate cortex (ACC), an integration hub for higher-order thalamic inputs important for social interaction. Humans with deletions including LMO4, an endogenous inhibitor of PTP1B, display intellectual disabilities and occasionally autism. PV-Lmo4KO mice ablate Lmo4 in PV interneurons and display ASD-like repetitive behaviors and social interaction deficits. Surprisingly, increased PV neuron-mediated peri-somatic feedforward inhibition to the pyramidal neurons causes a compensatory reduction in (somatostatin neuron-mediated) dendritic inhibition. These homeostatic changes increase filtering of mediodorsal-thalamocortical inputs but reduce filtering of cortico-cortical inputs and narrow the range of stimuli ACC pyramidal neurons can distinguish. Simultaneous ablation of PTP1B in PV-Lmo4KO neurons prevents these deficits, indicating that PTP1B activation in PV interneurons contributes to ASD-like characteristics and homeostatic maladaptation of inhibitory circuits may contribute to deficient information filtering in ASD.
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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.