Cited by 73Neuroendocrine regulation and behaviorAutism Spectrum Disorder ResearchGenetics and Neurodevelopmental Disorders

Parallel social information processing circuits are differentially impacted in autism

Open access
Lewis, Eastman M., Stein-O’Brien, Genevieve L., Patino, Alejandra V., Nardou, Romain, Grossman, Cooper D., Brown, Matthew, Bangamwabo, Bidii, Ndiaye, Ndeye +5 more·2020·Neuron

Published version of a preprint

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.

AI snapshot

Written from the paper’s full text.

TL;DR

Magnocellular and parvocellular oxytocin neurons form parallel social information processing streams in male mice. Parvocellular, but not magnocellular, oxytocin neurons are selectively required for peer-peer social reward learning and are enriched for autism risk genes and FMRP targets.

Key findings

  • In the PVN of male mice, 66% (952 ± 69) of oxytocinergic neurons were magnocellular and 34% (488 ± 25) parvocellular; magnocellular neurons were predominantly rostral and parvocellular neurons caudal.
  • Electrophysiological clustering matched anatomical classification: two k-means clusters corresponded 100% (18/18) with shoulder-based classification and 94% (17/18) with FluoroGold labeling; 4-AP reduced latency and increased action potential duration in magnocellular but not parvocellular OT neurons.
  • scRNA-seq of 194 collected OT neurons (146 passed QC) identified two transcriptional clusters; cluster 1 was 72.8% FG+ (magnocellular) and cluster 2 was 100% FG− (parvocellular). Differential expression found 181 genes at 0.1% FDR, including magnocellular-enriched Calb1 and Kcnmb4 and parvocellular-enriched Reln and Cnr1.
  • Fmr1 KO mice showed impaired peer-peer social CPP but normal cocaine CPP and alloparent CPP. NAc-projecting OT neurons were parvocellular (9/9; mean probability 92.8 ± 2.7%), and conditional Fmr1 deletion in NAc or OT neurons impaired social CPP, whereas Calb1-IRES-Cre::cdFmr1 KO mice were not impaired. ASD risk genes and FMRP targets were enriched in parvocellular relative to magnocellular OT neurons; schizophrenia risk genes were not enriched (p = 0.98).

Methods

  • Male mice (3–7 weeks; P30–40 for anatomy) were used with OT-2A-Flp::fdGFP, Fmr1 KO, conditional Fmr1 KO, and Calb1-IRES-Cre lines. Magnocellular OT neurons were labeled by i.v. FluoroGold; NAc projections were mapped with retrobeads and viral injections.
  • Electrophysiology used whole-cell current clamp in acute PVN slices, with post-hoc neurobiotin labeling and blind FG classification; k-means clustering was trained on electrophysiological features.
  • scRNA-seq used FACS-enriched OT neurons and modified SMART-Seq2, followed by UMAP, Monocle2 differential expression, and hypergeometric gene set enrichment. Behavior used social, cocaine, and alloparent conditioned place preference assays.

Limitations

  • The paper states that FluoroGold labeling has a non-zero false-negative rate and that FG− cells within the magnocellular transcriptional cluster may reflect technical artifact from acidic pH during dissociation/FACS rather than a biological subtype.
  • The paper states that no exclusively magnocellular OT projection was identified, so Calb1-IRES-Cre manipulation also knocked down Fmr1 in non-OTergic Calb1-expressing neurons elsewhere in the brain.
  • Evident from the text: experiments were conducted only in male mice, anatomical quantification used n = 3 mice, electrophysiology used n = 9 and n = 6 mice, and scRNA-seq analyzed 146 cells, so sex-specific and broader generalizability remain untested.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/j.neuron.2020.10.002

Cites

166 of 166 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 48 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    Autism risk genes are enriched in parvocellular compared to magnocellular oxytocin neurons.

    “autism risk genes are enriched in parvocellular compared to magnocellular oxytocin neurons”
    Quote in the paperSubstantial claim
  • Findingown data

    Unsupervised k-means clustering on electrophysiological features yields two clusters that correspond completely (100%, 18 of 18) with qualitative Sh classification.

    “The resulting best fit to this data are two clusters (Figure S2), which corresponded completely (100%, 18 of 18 OT neurons) with the qualitative magnocellular or parvocellular categorization based on the presence or absence of a shoulder in the electrophysiological trace (Figure 2P)”
    Quote in the paperSubstantial claim
  • Findingown data

    Parvocellular OT neurons are concentrated in the caudal division of the PVN.

    “parvocellular OT neurons are concentrated in the caudal division of the PVN”
    Quote in the paperSubstantial claim
  • Findingown data

    AP duration is longer in FG+ versus FG- OT neurons.

    “as well as longer in FG+ versus FG- OT neurons (Figure 2I)”
    Quote in the paperNot a substantial claim
  • Findingown data

    Oxt+ neurons in the rostral portion of the PVN were specifically colocalized with Calb1 and not Cnr1 mRNA.

    “Oxt+ neurons in the rostral portion of the PVN were specifically colocalized with Calb1 and not Cnr1 mRNA (Figure 4D)”
    Quote in the paperNot a substantial claim
  • May combine two claims. 25
  • Classified as probably not a substantial claim. 19
  • The quote only partly states this claim. 1
  • May combine two claims.

    Findingown data

    Application of 4-AP reduces the latency to first AP and increases AP duration in magnocellular (Sh+) OT neurons.

    “Application of the voltage-gated K+ channel blocker 4-AP (5 mM; Figures 2J,M) reduced the latency to first AP and increased AP duration in magnocellular (Sh+) OT neurons”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    Both WT and Fmr1 KO mice exhibit significant alloparent CPP.

    “as well alloparent CPP (aCPP) (Figures 5I-L, S4)”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    72.8% of cells in cluster 1 were FG positive, while cluster 2 contained only FG negative cells (100%) across all three replicates.

    “72.8% of cells in cluster 1 were FG positive (FG+), while cluster 2 contained only cells that were FG negative (FG-; 100%) across all three replicates (Figure S3)”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    In the PVN, 66% (952 ± 69 neurons) of OTergic neurons are magnocellular, while 34% (488 ± 25 neurons) are parvocellular.

    “in the PVN, 66% (952 ± 69 neurons) of OTergic neurons are magnocellular, while 34% (488 ± 25 neurons) of OTergic neurons are parvocellular (Figure 1G)”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    Among Sh+ OT neurons, 91% were FG+, and 100% of Sh- neurons were FG-.

    “among Sh+ OT neurons 91% were FG+, and 100% of Sh- neurons were FG- (Figure 2S)”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    Both WT and Fmr1 KO mice exhibit significant cocaine CPP.

    “while both WT and Fmr1 KO mice exhibit significant cocaine CPP (cCPP) (Figures 5E-H)”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    In the sampled neurons, 61% were Sh+ and 39% were Sh-.

    “61% of sampled neurons were Sh+, and 39% were Sh-”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    Among FG+ neurons, 100% were Sh+, and 88% of FG- neurons were Sh-.

    “100% of FG+ neurons were Sh+ and 88% of FG- neurons were Sh- (Figure 2T)”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    In the sampled neurons, 56% were FG+ and 44% were FG-.

    “56% of sampled neurons were FG+ and 44% were FG- (Figure 2R)”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    Peer-peer, but not filial social attachments are disrupted in the Fmr1 KO.

    “Specifically, peer-peer, but not filial social attachments are disrupted in the Fmr1 KO (Figure 5).”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    sCPP was absent in OT-2A-Flp::cdFmr1 KO, while WT animals injected with rgAAV-fdCre exhibited normal social reward learning.

    “sCPP was absent in OT-2A-Flp::cdFmr1 KO, while WT animals injected with rgAAV-fdCre exhibited normal social reward learning”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    The current studies provide validation of 8 of the 14 characteristics identified as distinguishing between magnocellular and parvocellular OT neurons, having discovered 2 of these characteristic features here.

    “In the current studies, we took a comprehensive approach to provide validation of 8 of the 14 characteristics identified as distinguishing between magnocellular and parvocellular OT neuron, having discovered 2 of these characteristic features here (Figure S8, Center; Figures 1–4, 8).”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    ASD risk genes and FMRP binding partners are significantly enriched in parvocellular relative to magnocellular OT neurons.

    “In both cases, genes were significantly enriched in parvocellular relative to magnocellular neurons (Figures 8A,B; Tables S3 and S4).”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Monogenic mutation of FMR1 is still the most common identified cause of ASD.

    “making monogenic mutation of FMR1, the gene disrupted in Fragile X (Verkerk et al., 1991), still the most common identified cause of the disease (Suhl and Warren, 2015)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Suhl and Warren, 2015

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Hypothalamic disruptions of OT neurons have been reported in human patients with ASD related disorders and in knockout mice for ASD risk genes including Fmr1, Cntnap2, and Pten.

    “hypothalamic disruptions of OT neurons have been reported in human patients with ASD related disorders such as Prader Willi syndrome (Swaab et al., 1995), as well as in knockout mice for ASD risk genes including Fmr1 (Francis et al., 2014), Cntnap2 (Peñagarikano et al., 2015), and Pten (Page et al., 2009)”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Swaab et al., 1995

      Not checked in the free run.

    • cites Francis et al., 2014 source

      Not checked in the free run.

    • cites Peñagarikano et al., 2015 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Evidence supporting a role for the genes encoding OXT and OXTR in ASD has been controversial.

    “evidence supporting a role for the genes encoding OT (OXT) and the OT receptor (OXTR) has been more controversial (Allen-Brady et al., 2009; Ebstein et al., 2009; Hovey et al., 2014; Satterstrom et al., 2020; Willsey et al., 2013; Zhang et al., 2017)”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites Allen-Brady et al., 2009 source

      Not checked in the free run.

    • cites Ebstein et al., 2009

      Not checked in the free run.

    • cites Hovey et al., 2014 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The etiology of ASD is primarily genetic.

    “The etiology of ASD is also primarily genetic (Sullivan et al., 2012)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Sullivan et al., 2012 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    50% of males and 20% of females with Fragile X meet full diagnostic criteria for ASD.

    “50% of males, and 20% of females with Fragile X meet full diagnostic criteria for ASD (Kaufmann et al., 2017)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Kaufmann et al., 2017 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    Magnocellular and parvocellular OT neuronal subtypes can be differentiated by a number of characteristic features.

    “magnocellular and parvocellular OT neuronal subtypes can be differentiated by a number of characteristic features (van den Pol, 2012)”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites van den Pol, 2012 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    Magnocellular neurons have increased mitochondrial density.

    “Previous reports indicate that magnocellular neurons have increased mitochondrial density (Dayanithi et al., 2012; van den Pol, 1982)”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites Dayanithi et al., 2012 source

      Not checked in the free run.

    • cites van den Pol, 1982 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    The social motivation theory of autism proposes that a primary deficit in peer-peer social reward learning could account for all characteristic behavioral impairments in ASD.

    “The social motivation theory of autism proposes that a primary deficit in peer-peer social reward learning could account for all of the characteristic behavioral impairments that define the clinical picture in ASD (Chevallier et al., 2013)”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Chevallier et al., 2013

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    Social reward learning impairments in Fmr1 KO mice are domain specific and restricted to peer-peer social attachments.

    “these findings support the view that social reward learning impairments in Fmr1 KO mice are domain specific and restricted to peer-peer social attachments”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationown data

    Social reward learning deficits in constitutive Fmr1 KO mice are not the consequence of hysteresis, but rather the ongoing requirement of Fmr1 in parvocellular, but not magnocellular OT neurons.

    “Taken together, these anatomical, electrophysiological, and functional genomic data demonstrate that social reward learning deficits seen in constitutive Fmr1 KO mice are not the consequence of hysteresis, but rather the ongoing requirement of Fmr1 in parvocellular, but not magnocellular OT neurons”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationreasoning

    Parallel processing enables a single peptide to encode a wide diversity of social behaviors, significantly expanding the network capabilities of the social brain.

    “Taken together these results delineate a novel example of parallel processing, which enables a single peptide to encode a wide diversity of social behaviors, significantly expanding the network capabilities of the social brain (Figure S8).”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationown data

    Fmr1 is required in parvocellular OT neurons, but not magnocellular OT neurons, for peer-peer social reward learning.

    “Furthermore, in parvocellular OT neurons (Figure 6), but not magnocellular OT neurons (Figure 4) Fmr1 is required for peer-peer social reward learning (Figure 7).”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationown data

    Cell type specific vulnerability of parvocellular OT neurons to genetic injury generalizes across multiple ASD etiologies, but is not apparent in unrelated genetic disorders that are not defined by impairments in social behavior.

    “These results support the view that cell type specific vulnerability of parvocellular OT neurons to genetic injury generalizes across multiple ASD etiologies, but is not apparent in unrelated genetic disorders that are not defined by impairments in social behavior.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationreasoning

    These findings provide improved face validity for social impairments in the Fmr1 KO mouse model of ASD and additional support for the social motivation theory of autism.

    “they provide improved face validity for social impairments in the Fmr1 KO mouse model of ASD, as well as additional support for the social motivation theory of autism”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Research into the pathogenesis of ASD has largely focused on understanding unifying biochemical mechanisms based on the hypothesis that ASD is a 'synaptopathy'.

    “For more than a decade, research into the pathogenesis of ASD has largely focused on understanding unifying biochemical mechanisms based on the hypothesis that ASD is a ‘synaptopathy’ (Bear et al., 2008; Dölen and Bear, 2009; Grabrucker et al., 2011).”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites Bear et al., 2008 source

      Not checked in the free run.

    • cites Dölen and Bear, 2009

      Not checked in the free run.

    • cites Grabrucker et al., 2011 source

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductown data

    Injection sites and viral function were confirmed.

    “Injection sites and viral function were confirmed as shown in Figure S6.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductnone given

    Calb1-Cre::cdFmr1KO experiments were done blind, as were a subset of OT-Flp::cdFmr1KO experiments.

    “Calb1-Cre::cdFmr1KO experiments were done blind, as were a subset of OT-Flp::cdFmr1KO experiments.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Neurons were targeted and recorded blind to FG labeling status.

    “Neurons were targeted and recorded blind to FG labeling status.”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductreasoning

    All OT-Flp mice used in these experiments were heterozygous, leaving one WT copy of the Oxt gene, to control for possible effects of knockin on Oxt gene function.

    “Therefore, in order to control for possible effects of knockin on Oxt gene function, all OT-Flp mice used in these experiments were heterozygous, leaving one WT copy of the Oxt gene.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    For k-means clustering analysis, two clusters were specified, as indicated by the elbow method.

    “For k-means clustering analysis, two clusters were specified, as this number of clusters was indicated by the elbow method (Figure S2).”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Exclusion criteria for sCPP were defined as a pre-conditioning preference score > 1.5 or < 0.5.

    “Exclusion criteria for this behavior were defined as a pre-conditioning preference score (timeside1/totaltime2) of > 1.5 or < 0.5.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Chamber assignments were counterbalanced for side and bedding cues in sCPP.

    “Chamber assignments were counterbalanced for side and bedding cues.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Injection sites were confirmed post-hoc by preparing sections containing the NAc.

    “Injection sites were confirmed post-hoc by preparing sections (20–50 μm) containing the NAc.”
    Quote in the paperNot a substantial claim
  • The quote only partly states this claim.

    Interpretationreasoning

    The anxiolytic effects of intranasal OT in Fragile X likely reflect indirect activity of OT in the periphery.

    “these anxiolytic effects likely reflect indirect activity of OT in the periphery.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductnone given

    All data were subjected to the Shapiro-Wilk normality test and F test to compare variances.

    “All data were subjected to the Shapiro-Wilk normality test and F test to compare variances.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Nine mice, with a maximum of 4 neurons per animal, were used to cross-validate FG and electrophysiological differentiation of magnocellular and parvocellular neurons.

    “Nine mice, with a maximum of 4 neurons per animal were used to cross-validate FG and electrophysiological differentiation of magnocellular and parvocellular neurons.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    146 neurons passed quality assessment.

    “146 neurons passed our quality assessment”
    Quote in the paperNot a substantial claim
40 of 40
  • The authors state this as an assumption.

    Little is known about the pathogenic mechanisms underlying social behavioral abnormalities in ASD and whether these are the consequence of selective vulnerability of specific cell types to genetic injury.

    “at this time little is known about the pathogenic mechanisms underlying social behavioral abnormalities in ASD, and whether these are the consequence of selective vulnerability of specific cell types to genetic injury”
  • The authors state this as an assumption.

    A quantitative analysis of the proportion and distribution of OT neuron subtypes within the PVN in mice has not been carried out to date.

    “to date a quantitative analysis of the proportion and distribution of these OT neuron subtypes within the PVN in mice has not been carried out”
  • The authors state this as an assumption.

    The FG tail vein injection labeling technique has a non-zero false negative rate.

    “The FG tail vein injection labeling technique, like all labeling techniques, has a non-zero false negative rate.”
  • The authors state this as an assumption.

    Calb1 is also expressed in the Purkinje cells of the cerebellum.

    “since Calb1 is also expressed in the Purkinje cells of the cerebellum”
4 of 4

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Lewis et al. (2020) used RNA-Seq to characterize the transcriptome of magno- and parvocellular PVN oxytocin neurons to examine common pathways linking oxytocin and ASD-related genes.

    “Lewis et al. (2020) recently used RNA-Seq to characterize the transcriptome of magno- and parvocellular PVN oxytocin neurons to examine common pathways linking oxytocin and ASD-related genes.”

    From Oxytocin, Neural Plasticity, and Social Behavior (2021) · cites this paper as Lewis et al. 2020

  • Single-cell transcriptomics studies show that paraventricular oxytocin neurons projecting within the brain that mediate social reward behaviors are disrupted in a mouse model of autism spectrum disorder, and those neurons are enriched for ASD-risk genes.

    “Single-cell transcriptomics studies show that PVN OXT neurons projecting within the brain that mediate social reward behaviors are disrupted in a mouse model of ASD, and those neurons are enriched for ASD-risk genes (159).”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Conflicting figure references for clustering training data

    Minor

    The statistical methods say the electrophysiological clustering algorithm was trained on neurons from Figure 1, whereas the Results say it was trained with electrophysiological data from Figure 2.

1 of 1

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Authors
Lewis, E. M., Stein-O’Brien, G. L., Patino, A. V., Nardou, R., Grossman, C. D., Brown, M., Bangamwabo, B., Ndiaye, N., Giovinazzo, D., Dardani, I., Jiang, C., Goff, L. A., & Dölen, G.
Affiliations
  • Johns Hopkins University (US)
  • University of Pennsylvania (US)
Corresponding author
  • Goff, Loyal A.
  • Dölen, Gül
Venue
Neuron
Publisher
Elsevier BV
Published
2020-11
Volume
108
Issue
4
Pages
659-675.e6
ISSN
0896-6273 (ISSN-L)
OpenAlex
W3094668538
Cited by
72
References
167
Citations by year
2026: 13 · 2025: 8 · 2024: 14 · 2023: 11 · 2022: 16 · 2021: 10
FWCI
10.11
Type
journal article
Language
en
Open access
Locations
  • Neuron (publishedVersion)
  • bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Chan Zuckerberg Initiative
  • National Institutes of Health
  • National Science Foundation
Topics
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
autism spectrum disorder, oxytocin neurons, magnocellular neurons, parvocellular neurons, Fmr1 knockout mice, autism risk genes, social information processing, electrophysiology, gene expression profiling
MeSH terms
Autism Spectrum Disorder, Animals, Disease Models, Animal, Male, Neurons, Object Attachment, Oxytocin, Social Behavior, Mice, Knockout, Mice, Fragile X Mental Retardation Protein, Fragile X Messenger Ribonucleoprotein 1, Gene Knock-In Techniques

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