Nitric oxide synthase inhibitors attenuate acute and chronic morphine withdrawal response in the rat locus coeruleus: an in vivo voltammetric study

Brain Research
S HallK Jhamandas

Abstract

Previous studies have demonstrated that activation of N-methyl-D-aspartate (NMDA) and non-NMDA receptors contributes to the hyperactivity of noradrenergic neurons of the locus coeruleus (LC) associated with opioid and non-opioid drug withdrawal syndromes. Using an in vivo voltammetric approach, we have examined the role of nitric oxide (NO), which mediates NMDA receptor function, in this withdrawal-induced LC hyperactivity. In the anaesthetized rat, acute morphine treatment (10 micrograms, i.c.v.) suppressed (55.7 +/- 4.4% of baseline) the catechol oxidation current (CA-OC) recorded from the LC using differential normal pulse voltammetry (DNPV). A subsequent intravenous injection of naloxone (2 mg/kg, i.v.) reversed the drug-induced inhibition of LC response and produced an increase (118.9 +/- 2.3% of baseline) in CA-OC above baseline, indicative of an acute withdrawal response. Systemic (100 mg/kg) and intracerebroventricular (i.c.v.) (100 micrograms) pretreatment of animals with the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) blocked the naloxone-induced LC withdrawal response without influencing the inhibitory effect of morphine on LC activity. In animals chronically infused with morphine (...Continue Reading

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Citations

May 3, 2007·Naunyn-Schmiedeberg's Archives of Pharmacology·María TorrecillaJoseba Pineda
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Nov 27, 1999·Annales Françaises D'anesthèsie Et De Rèanimation·A MullerJ P Loeffler

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