Lack of binding of acetaminophen to 5-HT receptor or uptake sites (or eleven other binding/uptake assays).
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-HT3 receptors. In the present study, we measured the affinity of acetaminophen at 5-HT3, as well as 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2, 5-HT2C, 5-HT4, 5-HT6, 5-HT7 and eleven other receptor sites and at serotonin and norepinephrine reuptake sites. At 10 microM, 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).
Raffa
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R.W. Johnson Pharmaceutical Research Institute, Spring House, PA 19477-0776, USA.
Codd
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D000082:Acetaminophen / Q000494:pharmacology*; D000818:Animals; D001667:Binding, Competitive; D002417:Cattle; D002540:Cerebral Cortex / Q000187:drug effects; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects; D051381:Rats; D011985:Receptors, Serotonin / Q000187:drug effects*; D013552:Swine
D011985:Receptors, Serotonin; D000082:Acetaminophen