ArticleCell2019
Targeting Peripheral Somatosensory Neurons to Improve Tactile-Related Phenotypes in ASD Models.
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Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 2 of them syntheses that pooled it.
0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 2 pooled it
13.9field-weighted citation impact, top 1% of its field
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Who cites it
150 citing papers in PubMed, 2 syntheses or guidelines pooled it, 254 citations in OpenAlex.
- Molecular insights into enriched environments and behavioral improvements in autism: a systematic review and meta-analysis.Frontiers in psychiatry · 2024Pooled it
- Exploring polygenic contributors to subgroups of comorbid conditions in autism spectrum disorder.Scientific reports · 2022Pooled it
- HD-tDCS effects on social impairment in autism spectrum disorder with sensory processing abnormalities: a randomized controlled trial.Scientific reports · 2025Trial
- Carotid body dysfunction contributes to respiratory instability in Rett syndrome.Current biology : CB · 2026Article
- A Developmental Neuroimmune Cascade Model of Autism Spectrum Disorder.International journal of molecular sciences · 2026Review
- Olfactory Valence-Processing Deficits and Aberrant Brain Network Connectivity Underlie Social Dysfunction in Shank3Neuroscience bulletin · 2026Article
- Region-specific microglial alterations in the acoustic startle circuit in Shank3 mice.Biochemistry and biophysics reports · 2026Article
- Microglia-Mediated Dysfunction of PKCγ Interneurons Underlies the Mechanical Hypersensitivity in Autism.Molecular neurobiology · 2026Article
- Autism associatedbioRxiv : the preprint server for biology · 2026Article
- Diminished Signal-to-Noise Ratio Disrupts Somatosensory Population Encoding and Drives Tactile Hyposensitivity in the Fmr1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cerebellar acceleration of learning in an evidence-accumulation task.Cell reports · 2026Article
- Shared and divergent alteration of whole-brain connectivity and sensory deficits in multiple autism mouse models.Molecular psychiatry · 2026Article
- Experience-dependent modulation of prosocial touch in mice.iScience · 2026Article
- Article
- Abnormal Neuronal Excitability and Reduced Parvalbumin Expression in Shank3-Deficient Parvalbumin Neurons of the Thalamic Reticular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- ImmatureProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Experience-dependent maturation of somatosensory parvalbumin interneurons during social development in prairie voles.Cerebral cortex (New York, N.Y. : 1991) · 2026Article
- Infant sensory gating and a developmental cascade to autistic traits and anxiety.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Dysfunctional neural dynamics associated with sensory phenotypes in Fragile X syndrome: insights from mouse models.Journal of neurodevelopmental disorders · 2025Review
- Improved albumin binding properties of Isoguvacine upon esterification as characterized by biophysical and computational tools.Scientific reports · 2025Article
90 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
Lauren L OreficeDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Jacqueline R MoskoDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Danielle T MorencyDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Michael F WellsMcGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, 43 Vassar Street, Cambridge, MA 02139, USA.
Aniqa TasnimDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Shawn M MozeikaDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Mengchen YeDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Anda M ChirilaDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Alan J EmanuelDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Genelle RankinDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Ryann M FameDepartment of Pathology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Maria K LehtinenDepartment of Pathology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Guoping FengMcGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, 43 Vassar Street, Cambridge, MA 02139, USA.
David D GintyDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. Electronic address: david_ginty@hms.harvard.edu.
Howard Hughes Medical Institute · USBoston Children's Hospital · USMcGovern Institute for Brain Research · US
Funding
Viral ModuleP30EY012196 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ZHIGANG HE · 1998 to 2026
$21.3MRes Support CoreP50MH094271 · NIMH · HARVARD UNIVERSITY · PI HENSCH, TAKAO K · 2011 to 2022
$18.6MElucidating Cutaneous Mechanosensory Circuits, from Development to DiseaseR35NS097344 · NINDS · HARVARD MEDICAL SCHOOL · PI GINTY, DAVID D · 2016 to 2023
$6.8MControl of neural stem cells by the nascent cerebrospinal fluidR01NS088566 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI LEHTINEN, MARIA · 2014 to 2024
$5.5MShank3 in Synaptic Function and AutismR01MH097104 · NIMH · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FENG, GUOPING · 2012 to 2016
$2.0MPediatric Pathology Translational ResearchT32HL110852 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI FLEMING, MARK D · 2012 to 2017
$1.4MUnderstanding Somatosensory Deficits in Autism Spectrum DisordersR00NS101057 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI OREFICE, LAUREN LYNN · 2019 to 2021
$824kThe role of autism susceptibility genes in the 16p11.2 locus on the development and function of human stem cell-derived neural cellsR00MH119327 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WELLS, MICHAEL FREDERICK · 2022 to 2024
$747kUnderstanding Somatosensory Deficits in Autism Spectrum DisordersK99NS101057 · NINDS · HARVARD MEDICAL SCHOOL · PI OREFICE, LAUREN LYNN · 2017 to 2018
$178kContribution of Peripheral Mechanoreceptor Subtypes to the Functional Organization of Mouse Primary Somatosensory CortexF32NS105324 · NINDS · HARVARD MEDICAL SCHOOL · PI EMANUEL, ALAN JOSEPH · 2018 to 2019
$105kThe Striatal Circuitry Underlying Autistic-Like BehaviorsF31MH098641 · NIMH · DUKE UNIVERSITY · PI WELLS, MICHAEL FREDERICK · 2012 to 2014
$96kHoward Hughes Medical InstituteNEI NIH HHS P30 EY012196NHLBI NIH HHS T32 HL110852NIMH NIH HHS F31 MH098641NIMH NIH HHS P50 MH094271NIMH NIH HHS R00 MH119327NIMH NIH HHS R01 MH097104NINDS NIH HHS F32 NS105324NINDS NIH HHS K99 NS101057NINDS NIH HHS R00 NS101057NINDS NIH HHS R01 NS088566NINDS NIH HHS R35 NS097344
Abstract
Somatosensory over-reactivity is common among patients with autism spectrum disorders (ASDs) and is hypothesized to contribute to core ASD behaviors. However, effective treatments for sensory over-reactivity and ASDs are lacking. We found distinct somatosensory neuron pathophysiological mechanisms underlie tactile abnormalities in different ASD mouse models and contribute to some ASD-related behaviors. Developmental loss of ASD-associated genes Shank3 or Mecp2 in peripheral mechanosensory neurons leads to region-specific brain abnormalities, revealing links between developmental somatosensory over-reactivity and the genesis of aberrant behaviors. Moreover, acute treatment with a peripherally restricted GABA
Indexed as
PhenotypeAction PotentialsAnimalsAnxietyAutism Spectrum DisorderBehavior, AnimalBrainDisease Models, AnimalFemaleGABA AgonistsIsonicotinic AcidsMaleMaze LearningMethyl-CpG-Binding Protein 2MiceMice, Inbred C57BLGABA AgonistsisoguvacineIsonicotinic AcidsMecp2 protein, mouseMethyl-CpG-Binding Protein 2Microfilament ProteinsNerve Tissue ProteinsShank3 protein, mouseASD therapeuticsautism spectrum disordersbrain developmentGABAmechanosensationmouse genetics
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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.