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The ventromedial hypothalamus (VMH) is a core structure underlying the generation of affective behaviors to threats. The prototypical threat to an individual is exposure to a noxious stimulus and the dorsomedial division of the VMH (dmVMH) receives nociceptive input. The present study evaluated the contribution of the dmVMH to generation of the affective reaction to pain in rats. Noxious tailshock elicits from rats vocalization afterdischarges (VADs) that have distinct spectrographic characteristics and are a validated model of the affective reaction to pain. VAD-like vocalizations (vocalizations with the same spectral characteristics of VADs) were elicited by stimulation (electrical or chemical) of the dmVMH. Stimulation in the vicinity of the dmVMH was ineffective in eliciting VADs. Manipulation of GABA(A) neurochemistry within the dmVMH altered the threshold for elicitation of VADs by dmVMH stimulation or tailshock. Administration of the GABA(A) antagonist bicuculline or the GABA(A) agonist muscimol into the dmVMH lowered and elevated VAD thresholds, respectively. These treatments did not alter thresholds of other tailshock elicited responses (vocalizations during tailshock or spinal motor reflexes). Bicuculline and muscimol administered into the dmVMH also elevated and lowered the asymptotic level of fear conditioning supported by dmVMH stimulation or tailshock. These findings demonstrate that the dmVMH contributes to the processing of pain affect and that the affective dimension of pain belongs to a broader class of sensory experience that represents threat to the individual.

Contribution of the ventromedial hypothalamus to generation of the affective dimension of pain