Evidence map›Paper›PMID 33113347›Full record

ArticleNeuron2020

Parallel Social Information Processing Circuits Are Differentially Impacted in Autism.

Eastman M Lewis, Genevieve L Stein-O'Brien, Alejandra V Patino, Romain Nardou, Cooper D Grossman, Matthew Brown, Bidii Bangamwabo, Ndeye Ndiaye, Daniel Giovinazzo, Ian Dardani and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuron, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed.

  1. Article
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  9. Oxytocin neurons in the anterior and posterior paraventricular nucleus have distinct behavioral functions and electrophysiological profiles.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  10. Article
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  12. Article
  13. Article
  14. Article
  15. Review
  16. Navigating Central Oxytocin Transport: Known Realms and Uncharted Territories.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Epigenomic and phenotypic characterization of DEGCAGS syndrome.European journal of human genetics : EJHG · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Eastman M LewisThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Brain Science Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Wendy Klag Institute for Autism and Developmental Disabilities, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Genevieve L Stein-O'BrienThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; Department of Oncology, Division of Biostatistics and Bioinformatics, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, School of Medicine, Baltimore, MD 21205; McKusick-Nathans Department of Genetic Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Alejandra V PatinoThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Brain Science Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Wendy Klag Institute for Autism and Developmental Disabilities, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; McKusick-Nathans Department of Genetic Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Romain NardouThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Brain Science Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Wendy Klag Institute for Autism and Developmental Disabilities, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Cooper D GrossmanThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Brain Science Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Matthew BrownThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Bidii BangamwaboThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Ndeye NdiayeThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Daniel GiovinazzoThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Ian DardaniDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.
Connie JiangCell and Molecular Biology Group, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA 19104, USA.
Loyal A GoffThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; McKusick-Nathans Department of Genetic Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA. Electronic address: loyalgoff@jhmi.edu.
Gül DölenThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Brain Science Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; The Wendy Klag Institute for Autism and Developmental Disabilities, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA. Electronic address: gul@jhu.edu.

Funding

Medical Scientist Training ProgramT32GM136577 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI ANDREA L COX · 2020 to 2026
$13.4M
Training Program in NeuroscienceT32NS091018 · NINDS · JOHNS HOPKINS UNIVERSITY · PI JAMES J KNIERIM, Daniel Hans O'Connor · 2015 to 2026
$4.1M
HopkinsPREP: Research, Community, Professional Training and Personal GrowthR25GM109441 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI WILSON, KATHERINE L · 2015 to 2024
$3.2M
Characterization of the role of Fmr1 in oxytocin neuronal subtypesR01MH117127 · NIMH · JOHNS HOPKINS UNIVERSITY · PI DOLEN, GUL · 2020 to 2024
$2.4M
Dissecting the role of vasopressin in regulating the critical period for social reward learningR01HD098184 · NICHD · JOHNS HOPKINS UNIVERSITY · PI DOLEN, GUL · 2020 to 2024
$1.7M
Characterization of a novel population of parvocellular oxytocin neurons controlling social reward learningR56MH115177 · NIMH · JOHNS HOPKINS UNIVERSITY · PI DOLEN, GUL · 2018 to 2019
$958k
NICHD NIH HHS R01 HD098184NIGMS NIH HHS R25 GM109441NIGMS NIH HHS T32 GM136577NIMH NIH HHS R01 MH117127NIMH NIH HHS R56 MH115177NINDS NIH HHS T32 NS091018
6 · The paper itself

Abstract

Parallel processing circuits are thought to dramatically expand the network capabilities of the nervous system. Magnocellular and parvocellular oxytocin neurons have been proposed to subserve two parallel streams of social information processing, which allow a single molecule to encode a diverse array of ethologically distinct behaviors. Here we provide the first comprehensive characterization of magnocellular and parvocellular oxytocin neurons in male mice, validated across anatomical, projection target, electrophysiological, and transcriptional criteria. We next use novel multiple feature selection tools in Fmr1-KO mice to provide direct evidence that normal functioning of the parvocellular but not magnocellular oxytocin pathway is required for autism-relevant social reward behavior. Finally, we demonstrate that autism risk genes are enriched in parvocellular compared with magnocellular oxytocin neurons. Taken together, these results provide the first evidence that oxytocin-pathway-specific pathogenic mechanisms account for social impairments across a broad range of autism etiologies.

Indexed as

Social BehaviorAnimalsAutism Spectrum DisorderDisease Models, AnimalFragile X Messenger Ribonucleoprotein 1Gene Knock-In TechniquesMaleMiceMice, KnockoutNeuronsObject AttachmentOxytocinFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1OxytocinautismcircuitFmr1Fragile Xhypothalamusnucleus accumbensoxytocinrewardsingle-cell RNA sequencingsocial

Identifiers

PMID33113347
PMCPMC8033501

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.