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Vol. 284, Issue 2, 455-459, February 1998

Lack of Morphine and Enkephalin Tolerance in 129/SvEv Mice: Evidence for a NMDA Receptor Defect

Yuri Kolesnikov , Subash Jain, Roger Wilson and Gavril W. Pasternak

The Cotzias Laboratory of Neuro-Oncology (Y.K., G.W.P.) and the Department of Anesthesiology (Y.K., S.J., R.W.), Memorial Sloan-Kettering Cancer Center, and The Departments of Neurology and Neuroscience and Pharmacology, Cornell University Medical College (G.W.P.), New York, New York

In contrast to the rapid development of tolerance to morphine in CD-1 mice, tolerance is not seen in 129/SvEv mice implanted with morphine pellets or given daily morphine injections for 5 days. Similarly, the progressive and complete loss of analgesia in CD-1 mice seen with repeated dosing of the delta ligand [D-Pen2,D-Pen5]enkephalin is not observed in 129/SvEv mice. In contrast, tolerance develops normally to both the kappa1 drug U50,488H and the kappa3 agent naloxone benzoylhdrazone. N-methyl-D-aspartate (NMDA) given alone attenuates morphine analgesia in CD-1 mice and accelerates the development of tolerance in CD-1 mice when given daily with morphine. In contrast, NMDA has no significant effect in the 129/SvEv mice in either paradigm. Activation of NMDA receptors can lead to the production of nitric oxide, which also is involved with morphine tolerance. Sodium nitroprusside and L-arginine increase nitric oxide levels and decrease morphine analgesia in both the control CD-1 and 129/SvEv mice. Thus, the defect in the NMDA/nitric oxide cascade responsible for the loss of morphine tolerance in the 129/SvEv mice rests at the level of the NMDA receptor itself or in the steps up to the activation of nitric oxide synthase.

0022-3565/98/2842-0455$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics


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