Pain-induced vocalization in the rat and its modification by pharmacological agents.

Vocalization was induced in rats by electrical stimulation of the tail (pain-induced vocalization), and its components were characterized in terms of latency, duration, frequency spectrum and energy. Noxious stimuli at threshold elicit a single vocalization component (V1). Increases in stimulus intensity produce additional discrete vocalization components (V2-Vn) with successively longer latencies, termed the vocalization afterdischarge (AD). The AD components are acoustically similar to each other but differ significantly from the V1 component. The duration, the specific acoustic measures and the sound energy of both V1 and AD components are positively correlated with intensity of the stimulus. The dependence of the V1 and AD components on the affective state of the rat was evaluated by comparing the acoustic characteristics of both components to those of stress-induced vocalizations, and by studying the effects of the anxiolytic drug diazepam and physical restraint on the threshold of V1 and AD. The AD components were markedly more dependent on the affective state of the rat then was the V1 component. A moderately low dose of morphine (3.0 mg/kg) also preferentially affected the AD component, suggesting that a significant portion of the action of morphine on pain-induced vocalization is mediated through its action on the affective state of the rat.