Chapter 7.4 - Hypothalamic control of pain vocalization and affective dimension of pain signaling

Abstract

Noxious tail-shock elicits vocalization afterdischarges (VADs) from rats that have distinct spectrographic characteristics and are a validated model of the affective response to pain. The ventromedial hypothalamus (VMH) is a core structure underlying the generation of affective behaviors to threats and receives nociceptive inputs. VAD-like vocalizations (vocalizations with the same spectral characteristics of VADs) are elicited by electrical or chemical stimulation of the dorsomedial-VMH. Pharmacological manipulation of GABAA receptors within the dorsomedial VMH altered the threshold for elicitation of VADs induced by this stimulation or by tail-shock, and altered the asymptotic level of fear conditioning supported by VMH stimulation or tail-shock. Partial kindling of the basolateral amygdala produced long-term increases in the amplitude of local field potentials recorded from the dorsomedial-VMH that correlated with long-term increases in VAD amplitude elicited by tail-shock. These findings demonstrate that the dorsomedial-VMH 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.