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• W1979831775 abstract "<h2>Abstract</h2> Previous studies have shown that administration of morphine results in alterations of splenic macrophage nitric oxide production. The present studies were conducted to determine the subtype of opioid receptor involved in the modulation of macrophage nitric oxide production. Moreover, the present work was directed at determining whether nitric oxide production is regulated through opioid receptors in the central nervous system (CNS) or via opioid receptors found directly on splenocytes. The study shows that intracerebroventricular (ICV) administration of the mu-selective opioid agonist, DAMGO, to rats dose-dependently increases the production of nitric oxide by splenocytes stimulated with toxic shock syndrome toxin (TSST-1). The effect of DAMGO is blocked by prior ICV administration of <i>N</i>-methylnaltrexone. In contrast, ICV administration of the kappa-selective agonist, U69,593, and the delta-selective agonist, DPDPE, have no significant effect on the production of nitric oxide. Furthermore, the in vitro administration of DAMGO, DPDPE, or U69,593 to splenocytes cultures does not significantly alter the production of nitric oxide by splenocytes. In addition, the present work shows that elevation of nitric oxide production by ICV administration of DAMGO produces functional changes in splenic lymphocytes. Collectively, these results indicate that mu-opioid receptors within the CNS are involved in the regulation of splenic nitric oxide production." @default.
• W1979831775 created "2016-06-24" @default.
• W1979831775 creator A5023043347 @default.
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• W1979831775 date "1998-08-01" @default.
• W1979831775 modified "2023-09-26" @default.
• W1979831775 title "Role of central mu-opioid receptors in the modulation of nitric oxide production by splenocytes" @default.
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• W1979831775 doi "https://doi.org/10.1016/s0165-5728(98)00128-3" @default.
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