Dipyrone analgesia in mice was potentiated by physostigmine, neostigmine and pilocarpine. This potentiation was antagonized by atropine sulfate and atropine methyl nitrate. Tremorine and dextroamphetamine which implicate brain monoamines in their analgesic effects, were inactive, as were carbachol and nicotine. Hydroxyzine did not potentiate dipyrone analgesia, ruling out a CNS depressant component in dipyrone potentiation. It was concluded that dipyrone which has central analgesic (Ruhnau, 1951) and parasympathomimetic effects (Lindner, 1956) is specifically potentiated by cholinergic drugs. Such potentiation of a non-narcotic analgesic by cholinergic agents argues against a specific involvement of cholinergic receptors in narcotics analgesia (and/or other narcotics' actions) and may indicate a cholinergic involvement in pain mechanisms and/or central analgesic effects without specific reference to narcotics.