Prior research suggests that afferent nociceptive information can directly activate the opioid and nonopioid brainstem antinociceptive systems. Grau (1987a) has hypothesized that direct activation occurs when an organism is exposed to severe aversive stimuli and that forebrain systems mediate the activation of the antinociception systems when mild aversive stimuli are used. The present experiments tested this hypothesis by examining the impact of spinalization and decerebration on the antinociception observed after mild (3 0.75-s 1.0-mA shocks) and vs. severe (3 25-s 1.0-mA shocks) tailshocks. It was found that spinal transection eliminated the antinociception observed after both shock schedules, whereas decerebration blocked mild shock-induced, but not severe shock-induced, antinociception. Surprisingly, decerebration potentiated severe shock-induced antinociception. The opioid antagonist naltrexone had no effect on the antinociception observed after severe shock in sham or decerebrate rats.
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