Volume 19, Issue 4 (December 2015)                   Physiol Pharmacol 2015, 19(4): 274-284 | Back to browse issues page

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Kamali M, Sahraei H, Khosravi M, Hassanpour S, Yaribeygi H. Asymmetric Involvement of Central and the Peripheral NMDA Glutamate Receptors in the Expression of Withdrawal Syndrome in Morphine-Dependent Mice. Physiol Pharmacol. 2015; 19 (4) :274-284
URL: http://ppj.phypha.ir/article-1-1134-en.html
Abstract:   (4285 Views)

Introduction: Morphine withdrawal syndrome is mediated via several central and peripheral neurological pathways. In the present study we investigated the role of N-methyl-D aspartic acid (NMDA) glutamate receptor on naloxone-induced withdrawal syndrome in morphine-conditioned mice. Materials and Methods: We designed two separate experiments. In experiment one, 30 male NMRI mice were divided into 5 groups, pretreated with memantine (0.1, 1 and 5 mg/kg; I.P.) followed by morphine-dependence period for 3 days. In the other experiment, 48 male NMRI mice distributed into 8 groups, pretreated with intra-accumbens (IAc) memantine (1 and 5 μg/animal) within the right, left and both side of nucleus accumbens (RNAcc, LNAcc and BNAcc) followed by I.P. morphine-dependence (3 days). On day 4, in both experiments, morphine was injected into mice, followed by naloxone. Then naloxone-induced total jumping count, jump height and defecation in morphine-conditioned mice were recorded for 30 min. Results: Pre-treatment by I.P. injection of memantine significantly attenuated naloxone precipitated jumping count/30 min, jumping height (mm) and fecal material output in morphine dependent mice (P<0.05). Also, IAC pretreatment with memantine in LNAcc, RNAcc and BNAcc significantly declined the effect of I.P. injection of naloxone on total jumping count and jumping height (P<0.05), pretreatment within memantine in LNAcc, RNAcc and BNAcc had no effect on defecation (P>0.05). Conclusion: These findings indicated asymmetric involvement of central and peripheral NMDA glutamate receptors in withdrawal syndrome development in morphine-dependent mice.

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