Analgesia followed by long-term hyperalgesia generated by disinhibition of the basolateral amygdala
Year: 2016
Type: dissertation
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.
Source: Human Biology
Author: Derek Atchley
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2561836037