Investigation of mechanisms and locus of neural change underlying stress-induced changes in affect

Blundell, Jacqueline (2001) Investigation of mechanisms and locus of neural change underlying stress-induced changes in affect. Masters thesis, Memorial University of Newfoundland.

[English] PDF (Migrated (PDF/A Conversion) from original format: (application/pdf)) - Accepted Version Available under License - The author retains copyright ownership and moral rights in this thesis. Neither the thesis nor substantial extracts from it may be printed or otherwise reproduced without the author's permission. Download (11MB) [English] PDF - Accepted Version Available under License - The author retains copyright ownership and moral rights in this thesis. Neither the thesis nor substantial extracts from it may be printed or otherwise reproduced without the author's permission. (Original Version)

Abstract

Stress has been linked to a variety of affective disorders, in particular, posttraumatic stress disorder (PTSD). PTSD is a long-lasting, chronic psychological disorder that results from exposure to a life threatening, inescapable stressor. There is no known cure or adequate treatment for this disease. In addition, there is little information regarding its cause. Brain imaging studies have implicated hyperexcitability of the right amygdala in PTSD and in response to traumatic events. Recent animal research has confirmed the role of the amygdala during severe stress. The goal of this study was to identify particular neural pathways and structures in which changes in function mediate particular changes in affect following predator stress. In this set of experiments, predator stress was achieved by exposing a rat to a cat for five minutes. -- Neural transmission of amygdala afferent and efferent pathways was examined in Experiment 1. Specifically, pathways studied were the ventral angular bundle input to the basolateral amygdala and central and basolateral amygdala output to the periaqueductal gray (PAG). Transmission was investigated one day (Day 1 study) and nine days (Day 9 study) after predator stress. Behavioral testing occurred seven days post predator stress in the Day 9 study. Predator stress was anxiogenic in the elevated plus maze, light/dark box and acoustic startle tests. -- Lasting changes were also observed in neural transmission in both the Day 1 and Day 9 studies. Predator stress appeared to potentiate right and depotentiate left hemisphere afferent amygdala transmission, in contrast, predator stress potentiated amygdala efferent transmission to both right and left PAG, depending on the amygdala nucleus stimulated. Paired pulse and intensity series analyses suggest that transmission changes may be post synaptic or presynaptic, depending on the pathway. These results are similar to results found in cat studies, but there are species differences. -- PCREB expression in the amygdala, PAG and ventral medial hypothalamus was examined in Experiment 2. Three groups were used in this experiment: Predator stressed (same procedure as used in electrophysioiogy study), Handled control and Restrained control. The restrained group was added to mimic the periods of immobility of cat exposed rats. -- Predator stress increased pCREB expression in the right lateral column of the PAG and a subset of nuclei in the amygdala. In addition, restraining the rat reduced pCREB expression in the left lateral and ventral columns of the PAG. There were no differences in pCREB intensity in the ventral angular bundle. -- Both experiments confirm the role of the amydala and PAG in predator stress- induced changes in affective behavior. In addition, as seen in cat and human data, these experiments appear to support the importance of the right hemisphere in stress.

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