title: Antinociceptive profiles of aspirin and acetaminophen in formalin, substance P and glutamate pain models.
abstract: Aspirin (ASA) is widely used oral analgesics and acts as an inhibitor of cyclo-oxygenase. Also, acetaminophen (APAP) is effective analgesics and may selectively inhibit brain prostaglandin synthetase. However, their mechanisms of action in CNS are poorly defined, although several authors have shown that the antinociceptive effects of ASA and APAP have different underlying mechanisms and play some possible roles on spinal nociceptive processing, such as inhibition of prostaglandin synthesis. To define and characterize antinociceptive profiles of ASA and APAP on various pain models, we performed intraplantar formalin injection test, intrathecal (i.t.) substance P (0.7 microg)-induced nociceptive response test, and i.t. glutamate (20 microg)-induced nociceptive response test after ASA or APAP (from 10 to 300 mg/kg) administered orally to the mouse. In the formalin test, ASA produced an antinociceptive effect during only the 2nd phase (20-40 min), but not the 1st phase (0-5 min), in a dose-dependent manner. However, APAP showed a dose-dependent antinociceptive effect during both phases of the formalin test. In addition, both ASA and APAP reduced nociceptive behavior induced by glutamate administered i.t. in a dose-dependent manner. In substance P-induced nociceptive response, APAP, but not ASA, showed antinociceptive effect in a dose-dependent manner. Our results suggest that ASA and APAP administered orally may be mediated by different nociceptive processing at the spinal cord level.
authors.affiliation: Department of Pharmacology, College of Medicine, Hallym University, 1 Okchundong, Chunchon, Kangwon-Do, 200-702, South Korea.
authors.forename: S S
authors.initials: SS
authors.lastname: Choi
authors.forename: J K
authors.initials: JK
authors.lastname: Lee
authors.forename: H W
authors.initials: HW
authors.lastname: Suh
mesh_terms: D000082:Acetaminophen / Q000494:pharmacology*; D018712:Analgesics, Non-Narcotic / Q000494:pharmacology*; D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions / Q000502:physiology; D005528:Foot / Q000294:innervation / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009619:Nociceptors / Q000187:drug effects / Q000378:metabolism; D010146:Pain / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D010147:Pain Measurement / Q000187:drug effects; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism; D018040:Receptors, Neurokinin-1 / Q000187:drug effects / Q000378:metabolism; D013116:Spinal Cord / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D013373:Substance P / Q000378:metabolism* / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D018712:Analgesics, Non-Narcotic; D016861:Cyclooxygenase Inhibitors; D017470:Receptors, Glutamate; D018040:Receptors, Neurokinin-1; D013373:Substance P; D000082:Acetaminophen; D018698:Glutamic Acid; D001241:Aspirin