Abstract
We have previously demonstrated that subcutaneous (s.c.) implantation of a 75-mg morphine pellet in a variety of mouse strains (including C3HeB/FeJ, C3H/HeJ, C57BL/6ByJ, C57BL/6J bgJ/bgJ and C57BL/6J bgJ/+ [Beige homozygous and heterologous mice]) suppresses the primary in vitro plaque-forming cell (PFC) response to sheep red blood cells (SRBCs), when spleen cells are harvested 48 hours after drug administration (1, 2). Involvement of opioid receptors in the immunosuppression is shown by two observations: (i) simultaneous implantation of a naltrexone pellet blocks the morphine-induced immunosuppression in C3H lineage mice, and (ii) morphine does not suppress the CXBK/By mouse strain, which is deficient in μ opioid receptors (1). While this evidence clearly supports the involvement of classical opioid receptors in C3H lineage mice, these in vivo studies cannot rule out a role for the hypothalamic-pituitary-adrenal (HPA) axis or for other mediators from other systems participating in the observed immunosuppression (3–5).
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Eisenstein, T.K., Meissler, J.J., Bussiere, J.L., Rogers, T.J., Geller, E.B., Adler, M.W. (1995). Mouse Strain Differences in in vivo and in vitro Immunosuppressive Effects of Opioids. In: Sharp, B.M., Eisenstein, T.K., Madden, J.J., Friedman, H. (eds) The Brain Immune Axis and Substance Abuse. Advances in Experimental Medicine and Biology, vol 373. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1951-5_16
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DOI: https://doi.org/10.1007/978-1-4615-1951-5_16
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