Functional aspects of bulbospinal monoaminergic projections in modulating processing of somatosensory information

Descending monoamine pathways have been shown to modulate the processing of nociceptive information. Several lines of evidence support this hypothesis: 1) stimulation of brain-stem sites by intracerebral electrodes or the local application of opiates inhibits spinal reflex activity, this effect being antagonized by intrathecal monoamine antagonists; 2) the iontophoretic administration of monoamines in the spinal cord will antagonize the discharge of dorsal horn nociceptors; and 3) the intrathecal administration of monoamines will elevate the pain threshold in the unanesthetized animal. One natural mode of activating this intrinsic circuit appears to be through the activation of small-diameter afferents. Recent evidence has shown that such somatic stimulation causes the release of 5-hydroxytryptamine and norepinephrine. The role of this system appears to be in modulating the properties of sensory processing at the spinal cord level.