Cheido M, Idova G
Laboratory of Mechanisms of Neurochemical Modulation, Institute of Physiology Siberian Branch of the Russian Academy of Medical Sciences, Novosibirsk.
Int J Immunopharmacol. 1997 Sep-Oct;19(9-10):529-33. doi: 10.1016/s0192-0561(97)00078-7.
The effects of substance P (SP) and its new structural analog EC-1 administered systemically to CBA mice on the immune responsiveness have been examined. Three main findings are presented in this study. First, the principal effect of SP and EC-1 on the immunity is a stimulatory one. It is shown that in the doses of 1, 10 and 100 mkg/kg of the body weight both neuropeptides significantly increased the number of plaque- and rosette-forming cells in the spleen of animals at the peak of the immune reactions. Second, the destruction of the pituitary stalk prevented the immune response stimulation caused by neuropeptides. Third, SP-induced immunostimulation was not observed after combination with the antagonist of the postsynaptic dopamine (DA) D-2 receptors haloperidol (2 mg/kg) suggesting the involvement of the DAergic system in the realization of this effect. Thus, these results demonstrate neurochemical DAergic mechanisms underlying the immunostimulating influence of tachykinins.
已研究了将P物质（SP）及其新的结构类似物EC-1全身给予CBA小鼠对免疫反应性的影响。本研究呈现了三项主要发现。第一，SP和EC-1对免疫的主要作用是刺激性的。结果表明，在体重剂量为1、10和100微克/千克时，两种神经肽在免疫反应高峰期均显著增加了动物脾脏中噬斑形成细胞和玫瑰花结形成细胞的数量。第二，垂体柄的破坏阻止了神经肽引起的免疫反应刺激。第三，与突触后多巴胺（DA）D-2受体拮抗剂氟哌啶醇（2毫克/千克）联合使用后未观察到SP诱导的免疫刺激作用，提示多巴胺能系统参与了这一效应的实现。因此，这些结果证明了速激肽免疫刺激作用背后的神经化学多巴胺能机制。
