 
        |
There
is now substantial evidence that perceptions of available social support
protect persons from pathogenic effects of depression and stressful events.
However, little is known about the neurobehavioral pathways that link social
support to improved physical and mental health outcomes. A growing literature
suggests that negative affect is associated with change in immune function
that may render the individual more susceptible to disease. In this
regard, it is widely proposed that activation of the HPA axis and the SAM
axis are biological pathways through which negative affect can influence
immune function and, in turn, increase disease risk. In this proposal
we begin to explore the possibility that one pathway by which social support
can protect persons from the pathogenic effects of negative life events
is via a reduction in HPA and SAM activity linked to activity of the hypothalamic
neurohormone, oxytocin. This hormone is associated with affiliative
behaviors in women and is known to down regulate the HPA and SAM stress
axes. By reducing activation along these pathways, oxytocin may buffer
the impact of stress on immune function and thus on disease processes,
accounting for observed associations between social support and improved
health outcomes in women. The proposed pilot study is designed to
provide a preliminary examination of the role of oxytocin in women's stress
sensitivity. Twenty-five normal cycling, depressed females aged 21-40
and 22 age-matched never-depressed controls will be recruited to participate
in a 3-hour laboratory experiment designed to stimulate, measure and compare
peripheral oxytocin release and basal oxytocin concentration within and
between groups, and to examine whether peripheral oxytocin release is associated
with a down regulation of activity along the HPA/SAM axes and a decrease
in stress-induced immune modulation following an acute stress task.
 (PDF
VERSION)(MS
WORD VERSION)
|
