Morphine-induced alterations of immune status are blocked by the dopamine D2-like receptor agonist 7-OH-DPAT.

Abstract 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) μ-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.