Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 148, Issue 1-2, Pages 54-62Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2003.11.006
Keywords
morphine; dopamine; immunomodulation; 7-OH-DPAT; natural killer cell activity; lymphocyte proliferation
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Funding
- NIDA NIH HHS [DA13371, DA07481, DA00334] Funding Source: Medline
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Morphine administration produces profound effects on the immune system, including reductions in natural killer cell activity, mitogen-induced lymphocyte proliferation, and cytokine production. Although it has been established that the activation of central nervous system (CNS) mu-opioid receptors by morphine induces immunomodulation, little is known about the neural mechanisms underlying such processes. Interestingly, it has been shown that the dopamine (DA) D-2-like receptor agonist 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT) blocks the effect of morphine on a number of behaviors that are mediated by central dopamine pathways. The present study examined whether dopamine is involved in the immunomodulatory effects of morphine. In separate experiments, 7-OH-DPAT was administered either systemically (subcutaneous, s.c.) or centrally (intracerebroventricularly, i.c.v.) prior to morphine treatment in male Lewis rats. The results demonstrate that both systemic and central administration of 7-OH-DPAT attenuate the suppressive effect of morphine on several measures of immune status. Overall, these findings provide the first evidence that CNS dopaminergic mechanisms are directly involved in morphine-induced immunomodulation. (C) 2003 Elsevier B.V. All rights reserved.
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