Abstract
The mechanism of analgesic action of acetaminophen (paracetamol) remains unknown. However, a central component distinct from that of the NSAIDs (non-steroidal antiinflammatory drugs) seems likely. A recent report ( NeuroReport 6:1546–1548, 1995) suggests the involvement of 5-HT 3 receptors. In the present study, we measured the affinity of acetaminophen at 5-HT 3, as well as 5-HT 1A, 5-HT 1B, 5-HT 1D, 5-HT 2, 5-HT 2C, 5-HT 4, 5-HT 6, 5-HT 7 and eleven other receptor sites and at serotonin and norepinephrine reuptake sites. At 10 μM, acetaminophen inhibited less than 10% specific radioligand binding at any site. These findings: (i) suggest that acetaminophen's effect on serotonergic pathways is indirect, and (ii) circumscribe acetaminophen's possible central analgesic mechanism(s).
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