Date of Award

Spring 1-1-2013

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Psychology & Neuroscience

First Advisor

Serge Campeau

Second Advisor

Heidi Day

Third Advisor

Gregory Carey

Fourth Advisor

Benjamin Greenwood

Fifth Advisor

Christopher Lowry

Abstract

The medial parvocellular nucleus of the paraventricular hypothalamic nucleus (mpPVN) mediates activation of the neuroendocrine hypothalamo-pituitary-adrenal (HPA) axis, elevating plasma corticosterone levels following stress. Similarly, the rostral region of the raphe pallidus (rRPa) mediates several stress-induced autonomic responses, including tachycardia. These autonomic and endocrine responses reliably undergo habituation following repeated exposures to the same stressor. Stress habituation is likely an important mechanism to keep physiological and psychological functions optimal in the face of repeated stress, however the central mechanisms underlying habituation are poorly understood. In order to determine whether effecter regions might be important for habituation of the responses that they control acutely, Chapter II describes an experiment in which the rRPa was inactivated with muscimol before three repeated exposures to noise stress. Inactivation of the rRPa attenuated the tachycardic response during acute loud noise compared to vehicle injected animals, and during a fourth drug free exposure animals in both treatment groups exhibited similar habituation of heart rate. This suggests that the rRPa is not necessary for habituation of tachycardia during repeated stress. A region capable of integrating stressor specific sensory information that projects to autonomic and endocrine effecter regions might be associated with stress response habituation. In the anatomical tract tracing study described in chapter III, it was determined that the mpPVN and the rRPa are innervated by the anterior portion of the posterior hypothalamus (aPH), and this region also displays high levels of stress-induced Fos following noise stress. In order to determine whether the aPH is necessary for stress habituation, Chapter IV describes experiments in which the aPH was inactivated with muscimol before three repeated exposures to loud noise or restraint stress. Inactivation of the aPH attenuated the acute endocrine response to both stressors compared to vehicle-injected controls, and in response to a fourth drug free exposure animals in the muscimol group did not display endocrine habituation. Based on the anatomical and functional evidence presented in this dissertation, it is suggested that the aPH may be an important region underlying the plasticity associated with stress habituation.

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