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Dysregulated cortisol has been linked to a variety of adverse physical and psychological consequences. Stressors in the childhood family environment can influence cortisol activity throughout development. For example, research has shown that both infants and children of depressed mothers exhibit altered levels of cortisol compared to infants and children of non-depressed mothers. It is unclear, however, whether exposure to maternal depression in childhood and adolescence is related to cortisol activity at later stages of development. The current study examined the longitudinal relation between maternal depressive symptoms during late childhood (9-12 years old) and adolescence (15-19 years old) and cortisol activity in offspring in young adulthood (24- 28 years old) in a sample of 40 young adults and their mothers. Maternal depressive symptoms were prospectively assessed at four time points across the 15 year study. Cortisol samples were collected from young adult offspring at the final time point. Findings revealed that higher levels of maternal depressive symptoms during late childhood were associated with lower total cortisol output in young adulthood. Results suggest that attenuated cortisol levels, which put these young adults at risk for a variety of stress-related physical and psychological illnesses, may be a long-term consequence of exposure to maternal depression,. Depressive symptoms in mothers during their child's adolescence, however, did not relate to cortisol output. These findings suggest a sensitive period in late childhood during which the development of HPA activity may be susceptible to the environmental stressor of maternal depression.
ContributorsMahrer, Nicole Eva (Author) / Wolchik, Sharlene (Thesis advisor) / Luecken, Linda (Thesis advisor) / Tein, Jenn-Yun (Committee member) / Arizona State University (Publisher)
Created2011
Description
Of the 2.87 million traumatic brain injuries (TBI) sustained yearly in the United States, 75% are diffuse injuries. A single TBI can have acute and chronic influences on the neuroendocrine system leading to hypothalamic-pituitary-adrenal axis (HPA) dysregulation and increased affective disorders. Preliminary data indicate TBI causes neuroinflammation in the hippocampus, likely due to axonal damage, and in the paraventricular nucleus of the hypothalamus (PVN), where no axonal damage is apparent. Mechanisms regulating neuroinflammation in the PVN are unknown. Furthermore, chronic stress causes HPA dysregulation and glucocorticoid receptor (GR)-mediated neuroinflammation in the PVN. The goal of this project was to evaluate neuroinflammation in the HPA axis and determine if GR levels change at 7 days post-injury (DPI).
Adult male and female Sprague Dawley rats were subjected to midline fluid percussion injury. At 7 DPI, half of each brain was post-fixed for immunohistochemistry (IBA-1) and half biopsied for gene/protein analysis. IBA-1 staining was analyzed for microglia activation via skeleton analysis in the hypothalamus and hippocampus. Extracted RNA and protein were used to quantify mRNA expression and protein levels for GRs. Data indicate increased microglia cell number and decreased endpoints/cell and process length in the PVN of males, but not females. In the dentate gyrus, both males and females have an increased microglia cell number after TBI, but there is also an interaction between sex and injury in microglia presentation, where males exhibit a more robust effect than females. Both sexes have significant decreases of endpoints/cell and process length. In both regions, GR protein levels decreased for injured males, but in the hippocampus, GR levels increased for injured females. Data indicate that diffuse TBI causes alterations in microglia morphology and GR levels in the hypothalamus and hippocampus at 7 DPI, providing a potential mechanism for HPA axis dysregulation at a sub-acute time point.
Adult male and female Sprague Dawley rats were subjected to midline fluid percussion injury. At 7 DPI, half of each brain was post-fixed for immunohistochemistry (IBA-1) and half biopsied for gene/protein analysis. IBA-1 staining was analyzed for microglia activation via skeleton analysis in the hypothalamus and hippocampus. Extracted RNA and protein were used to quantify mRNA expression and protein levels for GRs. Data indicate increased microglia cell number and decreased endpoints/cell and process length in the PVN of males, but not females. In the dentate gyrus, both males and females have an increased microglia cell number after TBI, but there is also an interaction between sex and injury in microglia presentation, where males exhibit a more robust effect than females. Both sexes have significant decreases of endpoints/cell and process length. In both regions, GR protein levels decreased for injured males, but in the hippocampus, GR levels increased for injured females. Data indicate that diffuse TBI causes alterations in microglia morphology and GR levels in the hypothalamus and hippocampus at 7 DPI, providing a potential mechanism for HPA axis dysregulation at a sub-acute time point.
ContributorsRidgway, Samantha (Author) / Thomas, Theresa C (Thesis advisor) / Newbern, Jason (Thesis advisor) / Bimonte-Nelson, Heather A. (Committee member) / Arizona State University (Publisher)
Created2019