Abstract
We report that the acetaminophen (paracetamol)-induced spinal (intrathecal, i.t.)/supraspinal (intracerebroventricular, i.c.v.) site/site antinociceptive 'self-synergy' in mice is attenuated by the opioid receptor subtype selective antagonists beta-funaltrexamine hydrochloride (beta-FNA; mu), naltrindole (delta), and nor-binaltorphine hydrochloride (nor-BNI; kappa). These findings further implicate endogenous opioids (viz., endorphins, enkephalins, and dynorphins) and their pathways as contributors to the central antinociceptive action of acetaminophen.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acetaminophen / administration & dosage
-
Acetaminophen / pharmacology*
-
Analgesics, Non-Narcotic / administration & dosage
-
Analgesics, Non-Narcotic / pharmacology*
-
Animals
-
Dynorphins / physiology
-
Endorphins / physiology
-
Enkephalins / physiology
-
Injections, Intraventricular
-
Injections, Spinal
-
Male
-
Mice
-
Mice, Inbred ICR
-
Naltrexone / analogs & derivatives*
-
Naltrexone / pharmacology
-
Narcotic Antagonists / pharmacology
-
Receptors, Opioid / drug effects*
-
Receptors, Opioid, delta / antagonists & inhibitors
-
Receptors, Opioid, kappa / antagonists & inhibitors
-
Receptors, Opioid, mu / antagonists & inhibitors
Substances
-
Analgesics, Non-Narcotic
-
Endorphins
-
Enkephalins
-
Narcotic Antagonists
-
Receptors, Opioid
-
Receptors, Opioid, delta
-
Receptors, Opioid, kappa
-
Receptors, Opioid, mu
-
Acetaminophen
-
norbinaltorphimine
-
Naltrexone
-
beta-funaltrexamine
-
Dynorphins
-
naltrindole