Reich, Lauren2019-10-142019-10-142019-05http://udspace.udel.edu/handle/19716/24466Stress is a common stimulus for both animals and humans. To process stressful stimuli, the hypothalamus-pituitary-adrenal (HPA) axis is crucial in the physiological cascade that produces glucocorticoid stress hormones: cortisol in humans and corticosterone in rodents. Glucocorticoids are essential for proper development, circadian rhythm, and behavior; however, overexpression of these hormones can result in damaging physiological and behavioral changes, often through the modification of transcription and the epigenome. Previous work in our lab has determined behavioral and epigenetic consequences in rodents exposed to our well-established seven-day caregiving behavioral paradigm of early-life adversity. External research has indicated a stress hyporesponsive period in infant rodents, where even in the presence of aversive and stressful stimuli, a pup’s HPA axis will not be activated. Here we test whether our aversive caregiving conditions evoke corticosterone production, as corticosterone could be involved in our previously discovered behavioral and epigenetic consequences of the caregiving paradigm. Results indicated no significant change in corticosterone levels based on treatment group or sex. These data are consistent with other work showing the lack of a corticosterone response to stressful and aversive stimuli during the stress hyporesponsive period, and suggests that our behavioral paradigm induces epigenetic, behavioral, and neurological changes without the influence of increased corticosterone.Biological sciences,Plasma corticosterone, Early-life adversityThesis