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NEUROPHARMACOLOGY

Role of the Nitric-Oxide Synthase Isoforms during Morphine-Induced Hyperthermia in Rats

Center for Substance Abuse Research and Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania

Recently, we demonstrated that the diffusible messenger molecule nitric oxide (NO) is involved in the hyperthermic response induced by morphine by using a nonselective nitric-oxide synthase inhibitor, N-nitro-L-arginine methyl ester. The present work extended these studies to include 7-nitroindazole (7-NI), an inhibitor specific for neuronal nitric-oxide synthase (nNOS), N(5)-(-iminoethyl)-L-ornithine (L-NIO), an inhibitor of endothelial NOS (eNOS), and aminoguanidine (AG), a potent inhibitor of inducible NOS (iNOS). A biotelemetry system was used in this study to measure the body temperature (Tb). A dose of 7-NI (5 or 10 mg/kg), which did not affect Tb by itself, blocked the hyperthermia induced by morphine in a dose-dependent manner (15 mg/kg i.p.). However, pretreatment with L-NIO (10–20 mg/kg) or with AG (50 mg/kg) failed to alter the hyperthermia induced by morphine. L-NIO (10–20 mg/kg) or AG (50 mg/kg) had no effect on Tb. These results suggest the involvement of nNOS in morphine-induced hyperthermia.

Address correspondence to: Dr. Khalid Benamar, Department of Pharmacology, Temple University School of Medicine, 3420 N. Broad Street, Philadelphia, PA 19140. E-mail address: kabenamar{at}hotmail.com

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