Abstract # 1775 Attenuation of opioid analgesia in T cell deficient mice

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• 作者：S. Rosen ; B. Ham ; M. Haichin ; I. Walters ; J.S. Mogil
• 刊名：Brain, Behavior, and Immunity
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：57
• 期：supp_S
• 页码：e20
• 全文大小：36 K

文摘

It is now known that neurons are not the only cell type involved in pain processing, which involves Schwann cells, satellite cells, and cells of the immune system, such as microglia, macrophages, and T cells. Many pain researchers have adopted the use of T-cell deficient mice in their experimental methods to elucidate the role of T-cells in neuropathic pain (Fitzgerald et al., 2009; Zuo et al., 2013), and T cells have been shown to release endogenous opioids (Dietrich et al., 2011). While it is well known that opioids have varying effects on the immune system, very little attention has been given to how the immune system may affect opioid regulation. We now have evidence that T-cell deficient mice (CD-1 nude and Rag1 null mutant) exhibit pronounced deficiencies in morphine analgesia, measured using the tail withdrawal or formalin test. Furthermore, T-cell deficient mice do not exhibit stress-induced analgesia after restraint. Adoptive transfer of splenocytes from CD-1 mice into T-cell deficient mice rescues opioid analgesia. These results suggest that T-cells play a role in opioid-mediated analgesia, not previously observed. Current experiments are investigating the mechanism behind this phenomenon.