Access Type

Open Access Thesis

Date of Award

January 2016

Degree Type

Thesis

Degree Name

M.A.

Department

Psychology

First Advisor

George S. Borszcz

Abstract

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.

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