Oxytocin, dopamine, and the amygdala: a neurofunctional model of social cognitive deficits in schizophrenia.

Rosenfeld, A. J.; Lieberman, J. A.; Jarskog, L. F.

doi:10.1093/schbul/sbq015

Cited by 178Schizophrenia research and treatmentNeuroendocrine regulation and behaviorNeurotransmitter Receptor Influence on Behavior

Oxytocin, dopamine, and the amygdala: a neurofunctional model of social cognitive deficits in schizophrenia.

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Rosenfeld, A. J., Lieberman, J. A., Jarskog, L. F.·2011·Schizophrenia Bulletin

DOI 10.1093/schbul/sbq015PMC PMC3160224

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Abstract

Until recently, the social cognitive impairment in schizophrenia has been underappreciated and remains essentially untreated. Deficits in emotional processing, social perception and knowledge, theory of mind, and attributional bias may contribute to functional social cognitive impairments in schizophrenia. The amygdala has been implicated as a key component of social cognitive circuitry in both animal and human studies. In addition, structural and functional studies of schizophrenia reproducibly demonstrate abnormalities in the amygdala and dopaminergic signaling. Finally, the neurohormone oxytocin plays an important role in multiple social behaviors in several mammals, including humans. We propose a model of social cognitive dysfunction in schizophrenia and discuss its therapeutic implications. The model comprises abnormalities in oxytocinergic and dopaminergic signaling in the amygdala that result in impaired emotional salience processing with consequent social cognitive deficits.

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Intranasal oxytocin (OXT) facilitates empathy.
“Converging evidence suggests that the hypothalamic neuropeptide oxytocin (OXT) facilitates empathy (Rosenfeld et al., 2011; Striepens et al., 2011; Riem, 2012).”
From Oxytocin Enhancement of Emotional Empathy: Generalization Across Cultures and Effects on Amygdala Activity (2018) · cites this paper as Rosenfeld et al., 2011

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Green MF, Penn DL, Bentall R, et al. Social cognition in schizophrenia: an NIMH workshop on definitions, assessment, and research opportunities. Schizophr Bull. 2008;34(6):1211- 1220.
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Authors: Rosenfeld, A. J., Lieberman, J. A., & Jarskog, L. F.
Affiliations: New York State Psychiatric Institute (US)
Corresponding author: Rosenfeld, A. J.
ORCID: Rosenfeld, A. J.
Lieberman, J. A.
Jarskog, L. F.
Venue: Schizophrenia Bulletin
Publisher: Oxford University Press (OUP)
Published: 2010-03-22
Volume: 37
Issue: 5
Pages: 1077-1087
ISSN: 0586-7614 (ISSN-L)
1745-1701
DOI: 10.1093/schbul/sbq015
PMC: PMC3160224
OpenAlex: W2109677536
Cited by: 178
References: 101
Citations by year: 2026: 3 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 16 · 2021: 12 · 2020: 9 · 2019: 11 · 2018: 10 · 2017: 15 · 2016: 7 · 2015: 21 · 2014: 20 · 2013: 18 · 2012: 11
FWCI: 8.53
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Schizophrenia Bulletin (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Eli Lilly and Company
Pfizer
AstraZeneca
GlaxoSmithKline
National Institutes of Health (5rc1mh089084-02)
National Institute of Mental Health (RC1 MH089084)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords: schizophrenia, social cognition
MeSH terms: Amygdala, Animals, Cognition Disorders, Dopamine, Emotions, Humans, Models, Psychological, Oxytocin, Schizophrenia, Schizophrenic Psychology, Social Behavior, Social Perception

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Oxytocin, dopamine, and the amygdala: a neurofunctional model of social cognitive deficits in schizophrenia.

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