By Herman Friedman (auth.), Herman Friedman, Toby K. Eisenstein, John Madden, Burt M. Sharp (eds.)
This quantity represents the court cases of the Symposium on AIDS, medicinal drugs of Abuse and the Neuroimmune Axis. This assembly was once held in San Diego, California, November 11-13, 1995. As within the earlier symposia during this sequence, efficient experiences have been reviewed in regards to the courting among the apprehensive and the immune platforms concerning the courting among medicines of abuse and infections, specifically infections through the immunode ficiency virus that motives AIDS. in recent times, quite a few investigators have began to explain the function of illicit medicines and their endogenous opposite numbers at the brain-immune axis. it's widely known that the neuroendocrine method is in detail fascinated by the results and manifestations of the interactions of gear of abuse and the immune process. The assembly on which the chapters during this publication are dependent introduced jointly many organic scientists from an array of assorted medical disciplines whose paintings is targeted at the results of gear of abuse at the neuroendocrine-immune axis and its relationships to immunodeficiency because of the AIDS virus. As some time past, the symposium used to be exact in concentrating on the . brain-immune axis from the point of view of substances of abuse instead of from the perspective of immunity or the mind itself.
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Additional resources for AIDS, Drugs of Abuse, and the Neuroimmune Axis
K. Cytokine-stimulated astrocytes damage human neurons via a nitric oxide mechanism. Glia in press. 19. , Sheng, W. , Peterson, P. , and Chao, C. C. (1995) Differential regulation by cytokines of production of nitric oxide by human astrocytes. Glia in press. 20. Choi, D. , and Visekul, V. (1988) Opioids and non-opioid enantiomers selectively attenuate N-methylD-aspartate neurotoxicity on cortical neurons. Eur. J. Pharmacol. 155: 27-35. 6 MORPHINE AFFECTS THE BRAIN-IMMUNE AXIS BY MODULATING AN INTERLEUKIN-l BETA DEPENDENT PATHWAY Sulie L.
And Peterson. K. Kappa opinid rcceptors in human Illicrnl'lia dO\\'Ilregulatc human immunodeficiency \·irtl,,-I e~pres,ion. Submilled. ]7. Lang. \IX .. Jourd·llcuil. D .. \1cddings .. B. and S\\·ain. (i. Increased opioid binding to p~riphL'ral \\'hit~ blood ccl],; in a ratmodcl oi'aclIlC CitOicstlhis. 5). IX ... \lIbin. 1' . ·d mammalian cells. J. lIis/oc/wlII. ('n()e/wlII. ' II 1<). Oi. '1'.. (ilazer.. '\. and Stry~r. I.. 'lIs ;lIld moiccules. J. (·elllh()l. 3:9x 1-I)X6 ( I'iX2J. 20. Chuang. I-..
Anti-inflammatory cytokines such as interleukin (IL)-4 have been shown to suppress murine microglial cell NO production (8). IL-4 also has been demonstrated to be protective against murine microglia-mediated neuronal injury (8). Several in vitro studies using murine cell cultures have shown that TGF-13, another anti-inflammatory cytokine, is neuroprotective (13, 14). Interestingly, we have found that morphine potentiates LPS-stimulated microglial cell release of TGF-13 (Fig. I). A potential mechanism underlying morphine-induced enhanced release of TGF-13 may involve morphine's ability to upregulate LPS-induced TNF-a , as reported previously (2).