Cited by 138Neuroendocrine regulation and behaviorNeuroinflammation and Neurodegeneration MechanismsAcute Ischemic Stroke Management

Oxytocin Mediates Social Neuroprotection After Cerebral Ischemia

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Karelina, Kate, Stuller, Kathleen A., Jarrett, Brant, Zhang, Ning, Wells, Jackie, Norman, Greg J., DeVries, A. Courtney·2011·Stroke

Abstract

Background and Purpose—: The reduced incidence, morbidity, and mortality of stroke among humans with strong social support have been well-documented; however, the mechanisms underlying these socially mediated phenomena remain unknown, but may involve oxytocin (OT), a hormone that modulates some aspects of social behavior in humans and other animals. Methods—: In the present study, adult male mice were socially isolated (housed individually) or socially paired (housed with an ovariectomized female); social pairing increased hypothalamic OT gene expression. To determine whether a causal relationship exists between increased OT and improved stroke outcome, mice were treated with exogenous OT or OT receptor antagonist beginning 1 week before induction of experimental stroke via middle cerebral artery occlusion. Results—: Relative to social isolation, social housing attenuated infarct size, neuroinflammation, and oxidative stress following experimental stroke; the neuroprotective effect of social housing was eliminated by receptor antagonist treatment. In contrast, administration of OT to socially isolated mice reproduced the neuroprotection conferred by social housing. We further report evidence for a direct suppressive action of OT on cultured microglia, which is a key instigator in the development of neuroinflammation after cerebral ischemia. Conclusions—: These findings support the hypothesis that OT mediates the neuroprotective effect of social interaction on stroke outcome.

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Crossref · 10.1161/strokeaha.111.628008

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Authors
Karelina, K., Stuller, K. A., Jarrett, B., Zhang, N., Wells, J., Norman, G. J., & DeVries, A. C.
Affiliations
The Ohio State University (US)
Venue
Stroke
Published
2011-12
Volume
42
Issue
12
Pages
3606-3611
ISSN
  • 0039-2499 (ISSN-L)
  • 1524-4628
OpenAlex
W2125030792
Cited by
138
References
41
Citations by year
2026: 4 · 2025: 8 · 2024: 5 · 2023: 18 · 2022: 16 · 2021: 16 · 2020: 10 · 2019: 15 · 2018: 10 · 2017: 8 · 2016: 12 · 2015: 2 · 2014: 8 · 2013: 2 · 2012: 3
FWCI
6.11
Type
journal article
Language
en
Open access
Locations
  • Stroke (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • American Heart Association
  • National Heart, Lung, and Blood Institute (R01HL080249)
  • National Institute of Neurological Disorders and Stroke (NS 045758, P30NS045758, R01NS40267-05, R01NS040267)
Topics
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
Keywords
oxytocin, social isolation, social housing, cerebral ischemia, neuroprotection, neuroinflammation, oxidative stress, microglia, oxytocin receptor, middle cerebral artery occlusion, infarct size, hypothalamus, social support
MeSH terms
Animals, Brain, Brain Ischemia, Female, Hormone Antagonists, Housing, Animal, Hypothalamus, Male, Oxytocin, Social Behavior, Social Isolation, Receptors, Oxytocin, Mice

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