Reference

Blockade of the discriminative effects of morphine in the rat by naltrexone and naloxone

Blockade of the discriminative effects of morphine in the rat by naltrexone and naloxone. Shannon, Harlan E.; Holtzman, Stephen G. (Dep. Pharmacol., Emory Univ., Atlanta, Ga.Except for chemicals metioned above, 52-26-6 and 1095-90-5 are also used., USA). Psychopharmacology (Berlin), 50(2), 119-24 (English) 1976. CODEN: PSCHDL. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) The capacity of the sp. narcotic antagonists naltrexone-HCl [16676-29-2] and naloxone-HCl (I-HCl) [357-08-4] to block the discriminative effects produced by morphine-HCl [52-26-6] in the rat were evaluated using a 2-choice, discrete-trial avoidance task. The antagonists produced a dose-dependent and time-dependent blockade of morphine's effects as measured by responding on the morphine-appropriate choice lever. Naltrexone and I were equipotent when given subcutaneously concomitantly with subcutaneously administered morphine. However, when the antagonists were administered orally at 0, 2, 4, or 8 h prior to s.c. morphine, naltrexone was more potent than I at every time point and had a duration of action at least twice that of oral I. The discriminitive effects of the narcotic analgesics morphine and methadone-HCl [1095-90-5] were also compared after oral and subcutaneous administration. Both drugs produced dose-related discriminative effects and were one-tenth as potent by the oral as by the subcutaneous route of administration. These results suggest that the discriminative effects produced by morphine in the rat can provide an animal model for the quant. evaluation of the narcotic antagonist properties of drugs that might be considered for use in narcotic antagonist maintenance programs for the treatment of narcotic addiction. .

Morphine-naloxone interaction in the central cholinergic system

Morphine-naloxone interaction in the central cholinergic system. The influence of subcortical lesioning and electrical stimulation. Jhamandas, K.; Sutak, M. (Fac. Med., Queen's Univ., Kingston, Ont., Can.). Br.Some commonly used reagents like 51-84-3 and 357-08-4 are used in this experiment. J. Pharmacol., 58(1), 101-7 (English) 1976. CODEN: BJPCBM. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Morphine [57-27-2] (2.5 mg/kg, i.v.) administered to rats inhibited the release of brain cortical acetylcholine (I) [51-84-3] by .apprx.50%; subsequent injection of naloxone-HCl [357-08-4] (0.1 mg/kg, i.v.) rapidly reversed the morphine inhibition producing a sustained I release nearly 200% greater than resting levels. Destruction of the medial thalamus abolished the inhibitory effects of morphine and its antagonism by naloxone. In normal rats, and to an even greater extent in morphine-dependent rats, naloxone (0.1 mg/kg, i.v.) increased the release of cortical I provoked by elec. stimulation of the medial thalamus or the reticular formation. Naltrexone-HCl [16676-29-2] also facilitated the elec.-stimulated release of cortical I. Morphine and naloxone could act at a subcortical site, probably the medial thalamus, to modify cortical I release. Naloxone may facilitate the elec.-induced release of I in the brain by antagonizing the effect of enkephalin. .