Arora P K, Hanna E E, Paul S M, Skolnick P
J Neuroimmunol. 1987 May;15(1):1-9. doi: 10.1016/0165-5728(87)90002-6.
24 h after administration of a single dose of the benzodiazepine receptor inverse agonists N'-methyl-beta-carboline-3-carboxamide (FG 7142) and 3-carbomethoxy-4-ethyl-6,7-dimethoxy-beta-carboline (DMCM), a profound suppression of the immune response was observed in rodents. This immunosuppression was manifest as a decrease in phytohemagglutinin (PHA) and concanavalin-A (Con-A) stimulated T cell proliferation in rats and mice administered FG 7142 and a decrease in allogeneic cytotoxic T lymphocyte activity in mice administered either FG 7142 or DMCM. The effects of FG 7142 were antagonized by the prior administration of Ro 15-1788, a benzodiazepine receptor antagonist. These findings demonstrate that the neural pathways subserved by benzodiazepine receptors can modulate immune function, and suggest that these receptors may be involved in the stress-induced modulation of immune function.
在给予单剂量苯二氮䓬受体反向激动剂N'-甲基-β-咔啉-3-甲酰胺（FG 7142）和3-甲氧羰基-4-乙基-6,7-二甲氧基-β-咔啉（DMCM）24小时后，在啮齿动物中观察到免疫反应受到显著抑制。这种免疫抑制表现为，在给予FG 7142的大鼠和小鼠中，植物血凝素（PHA）和刀豆蛋白A（Con-A）刺激的T细胞增殖减少；在给予FG 7142或DMCM的小鼠中，同种异体细胞毒性T淋巴细胞活性降低。苯二氮䓬受体拮抗剂Ro 15-1788预先给药可拮抗FG 7142的作用。这些发现表明，苯二氮䓬受体所支配的神经通路可以调节免疫功能，并提示这些受体可能参与应激诱导的免疫功能调节。
