Gavrilov Yu V, Perekrest S V, Novikova N S, Korneva E A
Department of General Pathology and Pathophysiology, Institute of Experimental Medicine, Russian Academy of Medical Sciences, 12 Academician Pavlov Street, 197376 St. Petersburg, Russia.
Neurosci Behav Physiol. 2008 Feb;38(2):189-94. doi: 10.1007/s11055-008-0028-9.
Stress is known to affect the intensity of the immune response. The involvement of central regulatory structures in mediating these changes was addressed by analyzing the extent of activation of neurons in the hypothalamus (in terms of the number of c-Fos-positive cells) in rats 2 h after i.v. administration of lipopolysaccharide alone and on the background of electrical pain stimulation. Studies were performed using 52 male Wistar rats weighing 200-250 g. c-Fos protein expression was studied by immunohistochemical analysis. Increases in the quantity of c-Fos-positive cells 2 h after administration of lipopolysaccharide were seen in the following hypothalamic structures: AHN, PVH, LHA, VMH, DMH, and PH. After electrical pain stimulation, the number of c-Fos-positive cells increased in these same hypothalamic structures (AHN, PVH, LHA, VMH, DMH, and PH). The combination of electrical pain stimulation and lipopolysaccharide administration led to a decrease in the extent of activation in hypothalamic structures AHN, PVH, LHA, and VMH as compared with the characteristic reaction to lipopolysaccharide without electrical pain stimulation. Electrical pain stimulation suppressed the intensity of the immune response induced by lipopolysaccharide (as assessed by local hemolysis and counts of the numbers of spleen antibody-forming cells). Thus, changes in the extent of activation of hypothalamic structures (AHN, PVH, LHA, VMH) correlated with the development of stress-induced immunosuppression, i.e., morphofunctional mapping of the extent of activation of hypothalamic structures allowed identification of which changes in hypothalamic cell activity occurred with stress-induced changes in immune system responses to antigen administration.
已知应激会影响免疫反应的强度。通过分析静脉注射脂多糖单独给药以及在电痛刺激背景下2小时后大鼠下丘脑神经元的激活程度（以c-Fos阳性细胞数量计），研究了中枢调节结构在介导这些变化中的作用。使用52只体重200 - 250克的雄性Wistar大鼠进行研究。通过免疫组织化学分析研究c-Fos蛋白表达。脂多糖给药2小时后，在下述下丘脑结构中观察到c-Fos阳性细胞数量增加：前下丘脑核（AHN）、室旁核（PVH）、外侧下丘脑区（LHA）、腹内侧核（VMH）、背内侧核（DMH）和乳头体核（PH）。电痛刺激后，这些相同的下丘脑结构（AHN、PVH、LHA、VMH、DMH和PH）中c-Fos阳性细胞数量增加。与无电痛刺激时脂多糖的特征性反应相比，电痛刺激与脂多糖给药相结合导致下丘脑结构AHN、PVH、LHA和VMH的激活程度降低。电痛刺激抑制了脂多糖诱导的免疫反应强度（通过局部溶血和脾抗体形成细胞数量计数评估）。因此，下丘脑结构（AHN、PVH、LHA、VMH）激活程度的变化与应激诱导的免疫抑制的发展相关，即下丘脑结构激活程度的形态功能图谱能够确定在应激诱导免疫系统对抗抗原给药反应发生变化时，下丘脑细胞活动发生了哪些变化。
