NO mediated increase of Fos protein and NMDA1A R mRNA expression in rat spinal cord during morphine withdrawal.
AIM: To investigate the effects of nitric oxide (NO) on activation of the rat spinal cord neurons during naloxone-precipitated morphine withdrawal. METHODS: Fos immunocytochemistry, NADPH-d histochemistry, Fos/NADPH-d double-labeling, intrathecal injection, antisense oligonucleotides (AS-ONs) techniques, and RT-PCR were used. RESULTS: Acute administration of naloxone and chronic administration of morphine did not change the expression of Fos protein and NADPH-d positive neurons, and there was no expression of Fos/NADPH-d double-labeled neurons in the spinal cord of rats. Morphine withdrawal increased the expression of Fos protein, NADPH-d positive, and Fos/NADPH-d double-labeled neurons, and they were observed in all the laminae of the rat spinal cord. Intrathecal injection of nNOS antisense oligonucleotides (nNOS-AS) inhibited the increase of Fos protein and NMDA(1A)R mRNA expression in the rat spinal cord during morphine withdrawal and decreased the scores of morphine withdrawal symptoms. The effect of nNOS-AS was greater than that of eNOS-AS. There was no effect in nNOS sense oligonucleotides (nNOS-S) group. CONCLUSION: NO mediated the increase of Fos protein and NMDA1A R mRNA expression in the rat spinal cord during morphine withdrawal.[1]References
- NO mediated increase of Fos protein and NMDA1A R mRNA expression in rat spinal cord during morphine withdrawal. Gao, J.L., Zeng, Y.M., Zhang, L.C., Gu, J., Liu, H.F., Zhou, W.H., Yang, G.D. Acta Pharmacol. Sin. (2001) [Pubmed]
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