Access Type

Open Access Thesis

Date of Award

January 2016

Degree Type


Degree Name




First Advisor

George S. Borszcz


Stress produces bimodal effects on pain peception. During exposure to a stressor pain responses are inibited (i.e. stress-induced analgesia). However, following long-term exposure to a stressor increases in responsiveness to painful stimuli may develop (i.e. stress-induced hyperalgesia). Here I evaluated how a key component of the subcortical defense circuit and target of stress hormones contributes to the development of both stress-induced analgesia and hyperalgesia. Bicuculline methiodide, a GABAA antagonist, injected into the basolateral amygdala was used to mimic the neural effects of a stressor or threat exposure. Immediately following injection pain responsiveness was decreased as measured by vocalizations after discharge and vocolizations during shock following a tailshock. In the days and weeks following bicuculline injection pain responsiveness became elevated compared to control rats. These findings suggest that pain responsiveness can be mediated by a reduction in GABAergic signalling within the basolateral amygdala following stress exposure.