The amygdala processes stimuli that threaten an individual and organizes the execution of learned and unlearned affective behaviors designed to cope with the threat. The prototypical threat to an individual is exposure to a noxious stimulus, and the amygdala is also involved in the processing and modulation of noxious stimulation. The central nucleus of the amygdala (CeA) receives nociceptive afferents and exhibits neuronal activation in response to noxious peripheral stimulation. Glutamate receptors in the CeA mediate this noxious-evoked neural excitation. The present study evaluated the behavioral antinociceptive action of the NMDA receptor antagonist AP-5 or the non-NMDA receptor antagonist CNQX administered into the CeA of rats. Pain behaviors organized at spinal (spinal motor reflexes = SMR), medullary (vocalizations during shock = VDS), and forebrain (vocalizations afterdischarges = VAD) levels of the neuraxis were elicited by tailshock. The threshold current intensity to elicit each behavior was determined following bilateral microinjections of AP-5 (1µg, 2µg, or 4µg in 0.25µl/side), CNQX (.25µg, .5µg, 1µg, or 2µg in 0.25µl/side) or vehicle into the CeA. Administration of AP-5 or CNQX into the CeA produced dose-dependent elevations in VAD and VDS thresholds, but failed to increase SMR threshold. These findings provide further evidence for the role of glutamatergic receptors in CeA in the suppression of pain behaviors organized at the supraspinal level of the neuraxis. As VADs are a validated rodent model of the affective dimension of pain, these findings also support the role of the CeA in the processing of pain affect. Supported by RO1 NS-045720 from NINDS