Experimental tooth movement is known to induce characteristic delayed and continuous nociception. Nociceptive somatic stimuli activate endogenous pain control systems such as descending monoaminergic pathways, which modulate the transmission of ascending sensory messages. To test the hypothesis that bulbospinal serotonergic pathways modulate subchronic nociception, we assayed the medulla at the level of the subnucleus caudalis and peri-aqueductal grey by high-performance liquid chromatography with electrochemical detection for the serotonin (5-hydroxytryptamine, 5-HT) and its metabolite (5-hydroxyindoleacetic acid, 5-HIAA) 24 hrs after the onset of experimental tooth movement. Experimental tooth movement significantly increased 5-HT and 5-HIAA levels, and 5-HIAA/5-HT, an index of serotonin turnover, in the medulla, and 5-HIAA level and 5-HIAA/5-HT in the peri-aqueductal grey, indicating that nociception induced by experimental tooth movement activates the bulbospinal serotonergic pathway.
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