An investigation into the impact of neuroimmune function after pregnancy or stress: Are there potential links to the onset of depression?
Date
2018
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Publisher
University of Delaware
Abstract
The National Institute of Mental Health has identified postpartum depression as one of several types of depression that affects 10-15% of mothers. It has previously been hypothesized that postpartum depression may be caused by dramatic changes in hormone levels that occur throughout pregnancy and the immediate postpartum period (Harris et al., 1994); however, the exact underlying mechanisms are still unknown. Like the dramatic change in hormone levels that occurs during and after pregnancy, the peripheral immune system is also altered during pregnancy to protect the developing semi-allogenic fetus from being rejected by the maternal immune system (Fallon et al., 2002). Despite this well-known phenomenon, the literature on how the central immune system is altered during pregnancy is still very limited. ☐ It is known that women are at a greater risk of developing postpartum depression if they have experienced depression during previous pregnancies (Patel et al., 2012). Thus, our first experiment sought to identify potential differences in postpartum anhedonia between first and second pregnancies. We have seen that female rats show significant anhedonia, measured by a decrease in sucrose preference, immediately after their first pregnancy (Posillico and Schwarz, 2016). In contrast, second-time mothers showed no significant anhedonia. ☐ The aim of the second experiment in this thesis was to identify a potential molecular basis for the onset of depressive-like behaviors caused by a first-time pregnancy and compare this to the effects of sub-chronic stress, also known to induce depressive-like behaviors. Increased circulating cytokines have been associated with numerous types of depression as well as chronic stress (Dantzer, 2009). Recently, we have found a significant increase in IL-6 expression in the female brain on the day of birth, or following sub-chronic stress (Posillico and Schwarz, 2016). Thus, we sought to determine whether blocking the function of this pro-inflammatory cytokine may prevent the anhedonia observed following a first-time birth or sub-chronic stress. Treatment with an IL-6 receptor antibody effectively attenuated depressive-like behavior immediately postpartum, but had no effect following sub-chronic stress. These results suggest that the molecular mechanisms that underlie the onset of anhedonia following birth and sub chronic stress may be distinct.
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Keywords
Biological sciences, Health and environmental sciences, Cytokine, Immunology, Postpartum depression, Pregnancy, Stress