Attenuation of morphine dependence and withdrawal by glycine(B) site antagonists in rats
by
Kotliska J.
Department of Pharmacodynamics,
Medical University School,
Staszica 4, PL-20-081,
Lublin, Poland
Pharmacol Biochem Behav 2001 Jan; 68(1):157-161 1999 Sep;124(1):51-5

ABSTRACT

Numerous data indicate that noncompetitive and competitive N-methyl-D-aspartate (NMDA) receptor antagonists inhibit the development of physical dependence on opioids when these substances are administered together, and NMDA receptor antagonists are used at lower range of doses. Higher doses of these antagonists can enhance some opioid-induced effects. The present study extends these findings to the effects of NMDA/glycine (glycine(B)) site antagonists. Wistar rats were rendered dependent on morphine by implantation of morphine pellets. Both of the glycine(B) site antagonists used, 7-chloro-4-hydroxy-3-(3-phenoxy)-phenyl-2(H)-quinolone (L-701,324; 2.5 and 5.0 mg/kg) and 5,7-dichlorokynurenic acid (5,7-DCKA; 25, 50, and 100 mg/kg), suppressed the expression of morphine withdrawal syndrome estimated as wet dog shakes. Furthermore, L-701,324 (2.5 and 5 mg/kg), given twice a day during the development of morphine dependence, attenuated the development of morphine dependence, and the results were comparable to those obtained after administration of noncompetitive NMDA receptor antagonist - MK801 (0.1 mg/kg). Our data suggest that glycine(B) site antagonists may attenuate wet dog shakes (withdrawal) and the development of dependence, both being induced by chronic morphine administration in rats.

NMDA
Arrestin
G protein
Morphine
Tramadol
Oxycodone
Mechanisms
Peroxynitrite
Receptor regulation
Fentanyl and ketamine
Signalling mechanisms
The extended amygdala
Opioids, mood and cognition
Morphine, naltrexone and tolerance
Tolerance, sensitization and dependence
The molecular mechanisms of opioid tolerance
Anxiety, opioids, cholecystokinin and tolerance

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