Access Type

Open Access Dissertation

Date of Award


Degree Type


Degree Name




First Advisor

George S. Borszcz


The amygdala processes stimuli that threaten an individual and organizes the execution of affective behaviors designed to cope with the threat. The prototypical threat to an individual is exposure to a noxious stimulus. The central nucleus of the amygdala (CeA) receives nociceptive afferents and exhibits neuronal activation in response to noxious peripheral stimulation. NMDA receptors within CeA mediate this noxious-evoked neural excitation, and previous studies in the laboratory have shown that blockade of CeA NMDA receptors via the antagonist APV elevates the threshold for noxious tail-shock-induced vocalization afterdischarges (VADs), a validated measure of pain affect in the rat. The present study further evaluated the contribution of NMDA receptors to the suppression of pain affect.

Intra-CeA NMDA receptor activation via the agonist NMDA elevated VAD thresholds in a dose dependent manner. That the NMDA receptor agonist and antagonist produce similar behavioral effects is hypothesized as the result of targeting separate neural populations within the CeA. Whereas the antagonist likely inhibits nociception at the level of the lateral capsular division of the CeA, the agonist likely activates antinociceptive efferents at the level of the vlPAG. In support of this hypothesis, the present study revealed that Fos expression within vlPAG is greater in rats that received intra-CeA agonist NMDA treatment compared to those that received the antagonist APV or saline. Lastly, intra-CeA NMDA agonist-induced elevations in VAD thresholds were blocked via the pre-treatment of the vlPAG with the mu-opiate antagonist CTAP. These studies provide the first demonstration of the contribution of CeA NMDA receptors to the generation of pain affect in the rat.