Sei Y, McIntyre T D, Fride E, Yoshimoto K, Skolnick P, Arora P K
Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
NIDA Res Monogr. 1990;105:524-9.
Administration of morphine as a subcutaneous implant inhibits the initial influx of calcium (Ca2+) induced by mitogens in mouse splenocytes. This effect was not reproduced by incubation of splenocytes with morphine (10(-8)-10(-4)M). Within T cell subpopulations, CD4+, but not CD8+ cells were affected. Adrenalectomy abolished this effect of morphine in CD4+ but not B cells. Moreover, simultaneous administration of the opiate antagonist naltrexone blocked the effect of morphine in B cells, but not in CD4+ cells. These data indicate that inhibition of Ca2+ influx by morphine may be mediated through distinct glucocorticoid-dependent and independent mechanisms. The morphine-induced inhibition of Ca2+ influx in immune cells reported here may be an early event mediating opiate-induced immunosuppression.
皮下植入吗啡可抑制丝裂原诱导的小鼠脾细胞中钙（Ca2+）的初始内流。用吗啡（10(-8)-10(-4)M）孵育脾细胞未重现此效应。在T细胞亚群中，CD4+细胞而非CD8+细胞受到影响。肾上腺切除术消除了吗啡对CD4+细胞而非B细胞的这种作用。此外，同时给予阿片拮抗剂纳曲酮可阻断吗啡对B细胞的作用，但对CD4+细胞无此作用。这些数据表明，吗啡对Ca2+内流的抑制可能通过不同的糖皮质激素依赖性和非依赖性机制介导。本文报道的吗啡诱导的免疫细胞中Ca2+内流抑制可能是介导阿片诱导的免疫抑制的早期事件。
