Social environment contributes to individual differences in the incidence and symptomology of a wide range of human health conditions, including depression, cancer, cardiovascular disease, cerebrovascular disease, wound healing, and neuropathic pain. Our laboratory and others have successfully recapitulated the exacerbating effects of social isolation on outcome in rodent models of these disorders; a common physiological feature of each of these conditions is increased neuroinflammation among socially isolated animals relative to socially housed animals. In turn, neuroinflammation is associated with greater physical and psychological morbidity, although the physiological link between social behavior and neuroinflammation is not known. We propose that oxytocin, a hormone that is released by social interaction, provides a protective function by suppressing the activation of microglia. The specific hypothesis tested in this proposal is that oxytocin reduces the expression of proinflammatory cytokines in the brain by suppressing microglial activation. Converging evidence of oxytocin modulation of microglia will be provided through in vivo and in vitro experiments. The data collected as part of this proposal will increase our understanding of how variation in social environment can impact health. Identification of the physiological factors underlying social influences on health could facilitate the development of therapeutic approaches that improve health measures among people with impoverished social environments.

Public Health Relevance

Social environment has a strong influence on health. The overarching goal of this proposal is to provide insights into the physiological changes that occur in the brain following social isolation. This research has the potential to benefit individuals who are socially isolated and at increased risk for developing health complications.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Exploratory/Developmental Grants (R21)
Project #
1R21MH107002-01A1
Application #
8986296
Study Section
Biobehavioral Regulation, Learning and Ethology Study Section (BRLE)
Program Officer
Desmond, Nancy L
Project Start
2015-05-18
Project End
2017-02-28
Budget Start
2015-05-18
Budget End
2016-02-29
Support Year
1
Fiscal Year
2015
Total Cost
Indirect Cost
Name
Ohio State University
Department
Neurosciences
Type
Schools of Medicine
DUNS #
832127323
City
Columbus
State
OH
Country
United States
Zip Code
43210
Gaudier-Diaz, Monica M; Haines, Adam H; Zhang, Ning et al. (2018) Social influences on microglial reactivity and neuronal damage after cardiac arrest/cardiopulmonary resuscitation. Physiol Behav 194:437-449
Gaudier-Diaz, Monica M; Zhang, Ning; Haines, Adam H et al. (2017) Social interaction modulates the neuroinflammatory response to global cerebral ischemia in male mice. Brain Res 1673:86-94