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MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA

Karelina, Ekaterina
http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479

Abstract Details

2010, Doctor of Philosophy, Ohio State University, Neuroscience.
Social isolation has long-term physiological and psychological consequences. The benefits associated with social support are well described in cerebrovascular disease patients; however, the mechanisms by which social interactions influence disease outcome are unknown. The present body of work examined the effects of social interaction on stroke outcome in mice. The goals of this dissertation are to describe the phenomenon and consequences of social interaction-mediated neuroprotection in a mouse model of cerebral ischemia, as well as to describe a neuroendocrine basis by which social interactions may mediate stroke-induced neuroinflammation and functional outcome. Social housing conditions influence measures of stroke outcome in a mouse model of transient focal cerebral ischemia. Male mice housed with an ovariectomized female have attenuated ischemic injury, improved post-stroke survival rate and enhanced functional recovery. Importantly, this neuroprotective effect requires the physical contact component of social interaction, as removal of this component using a barrier (while preserving all other sensory stimuli associated with social interactions), eliminates both the neuroprotection and locomotor recovery in socially housed mice. Additionally, the reduction in ischemic damage in socially housed mice is accompanied by an anti-inflammatory response, characterized by altered central and systemic markers of inflammation. Specifically, interleukin-6, a cytokine that is both modified by social interactions and predicts stroke outcome, is differentially regulated in socially housed and isolated mice, suggesting that social housing may alter the trajectory of ischemia outcome in part by attenuation of inflammation. Finally, the role of oxytocin, a neuropeptide released during social contact, was assessed as a potential mediator of social neuroprotection. Administration of oxytocin to socially isolated animals reproduces the neuroprotection conferred by social housing, and blockade of oxytocin action via administration of an oxytocin receptor antagonist blocks these effects in socially housed animals. Importantly, oxytocin receptors on microglia, critical immune effectors in ischemia, appear to modulate microglia activation in response to an inflammatory stimulus. These findings support the hypothesis that oxytocin is neuroprotective against physiological and behavioral consequences of cerebral ischemia, and provide insight into the mechanism by which social influences impact stroke outcome.
Courtney DeVries (Advisor)
Randy J. Nelson (Committee Member)
Jonathan P. Godbout (Committee Member)
Amy E. Lovett‐Racke (Committee Member)
Neurology
social interaction; stroke; oxytocin

Recommended Citations

Citations

  • Karelina, E. (2010). MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479

    APA Style (7th edition)

  • Karelina, Ekaterina. MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA. 2010. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479.

    MLA Style (8th edition)

  • Karelina, Ekaterina. "MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA." Doctoral dissertation, Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479

    Chicago Manual of Style (17th edition)

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This open access ETD is published by The Ohio State University and OhioLINK.