Oxytocin, sexually dimorphic features of the social brain, and autism
Abstract
The common features of autism spectrum disorder, a highly heritable representative pervasive developmental disorder with significant heterogeneity and multiple-genetic factors, are severe dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in the female gender. Concomitantly, certain domains of mental function, such as emotional memory and social reciprocity, show a significant sex difference. In addition, recent neuroimaging studies have shown significant sexual dimorphisms in neuroanatomical correlates of social cognition. Recently, some sexually dimorphic factors, including oxytocin, vasopressin, and genes linked with the x-chromosome, have received attention because of their possible contribution to mental development especially in the social cognitive domain. Taking this evidence together, it is hypothesized that a sexually dimorphic factor associated with social reciprocity could affect characteristics of autism spectrum disorder including dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in female gender. This review article overviews sexual dimorphisms in clinical features of autism spectrum disorder, in normal social cognition, and in social brain function and structure. The association of oxytocin with sexual dimorphisms, social reciprocity, neural correlates of social cognition, and the pathogenesis of autism spectrum disorder were further summarized. Recent studies have suggested that oxytocin plays a role in social attachment in experimental animals, in enhancing social interactive ability in human adults, and in the pathogenesis of autism spectrum disorder. Thus, the ongoing accumulated evidence suggests that oxytocin deserves to be examined as a candidate that causes the sexually dimorphic aspect of human social reciprocity, social brain development and the pathogenesis of autism spectrum disorder.
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OT can contribute to the pathophysiology of ASD and could be a candidate therapeutic agent for the symptoms of ASD.
“it was suggested that OT can contribute to the pathophysiology of ASD, a sexually dimorphic neurodevelopmental disorder with social deficits as a core feature, and that it could be a candidate thera-peutic agent for the symptoms of ASD (Yamasue et al., 2009).”
From Integrative Approaches Utilizing Oxytocin to Enhance Prosocial Behavior: From Animal and Human Social Behavior to Autistic Social Dysfunction (2012) · cites this paper as Yamasue et al., 2009
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“Both oxytocin (OT) and vasopressin (AVP) are known to modulate social behavior, and dysfunction in both systems has been postulated as a potential cause of various psychiatric disorders involving social behavioral deficits (Goodson and Thompson, 2010; Meyer-Lindenberg et al., 2011; Yamasue et al., 2009).”
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REVIEW: Oxytocin: Crossing the Bridge between Basic Science and Pharmacotherapy
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Two genetic variants of CD38 in subjects with autism spectrum disorder and controls
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Self-citationIntranasal administration of oxytocin: behavioral and clinical effects, a review
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Association between the oxytocin receptor gene and amygdalar volume in healthy adults
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Self-citationThe orgasmic history of oxytocin: Love, lust, and labor
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Oxytocin and Autism Spectrum Disorders
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Self-citationVasopressin Boosts Placebo Analgesic Effects in Women: A Randomized Trial
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CD38 and its role in oxytocin secretion and social behavior
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Diminished Medial Prefrontal Activity behind Autistic Social Judgments of Incongruent Information
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The Roles of Oxytocin and CD38 in Social or Parental Behaviors
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Cd38 Gene Knockout Juvenile Mice: A Model of Oxytocin Signal Defects in Autism
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- Authors
- Yamasue, H., Kuwabara, H., Kawakubo, Y., & Kasai, K.
- Affiliations
- The University of Tokyo (JP)
- Corresponding author
- Yamasue, Hidenori
- Venue
- Psychiatry and Clinical Neurosciences
- Publisher
- Wiley
- Published
- 2009-03-20
- Volume
- 63
- Issue
- 2
- Pages
- 129-140
- ISSN
- 1323-1316 (ISSN-L)
- 1440-1819
- OpenAlex
- W1924974749
- Cited by
- 78
- References
- 104
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 5 · 2022: 3 · 2021: 2 · 2020: 5 · 2019: 3 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 7 · 2014: 3 · 2013: 10 · 2012: 11
- FWCI
- 1.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychiatry and Clinical Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- 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
- oxytocin, autism spectrum disorder, sexual dimorphism, social brain, social reciprocity, social cognition, vasopressin, sex differences, social attachment, social brain development, autism pathogenesis, X-linked genes
- MeSH terms
- Animals, Autistic Disorder, Brain, Cognition, Female, Humans, Male, Oxytocin, Sex Characteristics, Social Behavior
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