Shimizu N, Hori T, Nakane H
Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Brain Behav Immun. 1994 Mar;8(1):14-23. doi: 10.1006/brbi.1994.1002.
The purpose of this study was to investigate whether an intraperitoneal injection of interleukin-1 beta (IL-1 beta) affects noradrenaline release in the spleen through its action on the brain of conscious rats. An in vivo microdialysis technique consisting of high-performance liquid chromatography with electrochemical detection was used for chronic monitoring of the splenic noradrenaline. The perfusion of a high concentration of K+ Ringer solution through the microdialysis probe significantly increased the concentration of noradrenaline in the spleen, while a perfusion of either Ca(2+)-free or tetrodotoxin-containing Ringer solution decreased the noradrenaline level in the dialysate. These results indicate that the noradrenaline recovered in the splenic dialysate is mainly derived from the nerve terminals of the splenic sympathetic nerve. The intraperitoneal injection of IL-1 beta (100 ng/kg) produced an immediate and significant increase in the noradrenaline levels in the spleen. The increased level reached a maximum level 40 min after injection and then gradually returned to the basal level. An intracerebroventricular (ICV) injection of a corticotropin-releasing factor (CRF) antagonist (alpha-helical CRF9-41, 30 micrograms) significantly attenuated the IL-1 beta-induced increase in the noradrenaline release. An ICV injection of CRF (2 micrograms) also caused a significant increase in splenic noradrenaline, which showed two distinct peaks at 20 and 140 min, respectively. These results suggest that the intraperitoneal injection of IL-1 beta facilitates noradrenaline release in the spleen through activation of the sympathetic nerve, and the increased sympathetic activity is, at least in part, due to the excitation of neurons containing CRF in the brain.
本研究的目的是调查腹腔注射白细胞介素-1β（IL-1β）是否通过作用于清醒大鼠的大脑来影响脾脏中去甲肾上腺素的释放。采用高效液相色谱-电化学检测的体内微透析技术对脾脏去甲肾上腺素进行长期监测。通过微透析探针灌注高浓度的K⁺林格溶液可显著提高脾脏中去甲肾上腺素的浓度，而灌注无Ca²⁺或含河豚毒素的林格溶液则会降低透析液中去甲肾上腺素的水平。这些结果表明，脾脏透析液中回收的去甲肾上腺素主要来源于脾交感神经的神经末梢。腹腔注射IL-1β（100 ng/kg）可使脾脏中去甲肾上腺素水平立即显著升高。注射后40分钟，升高水平达到最大值，然后逐渐恢复到基础水平。脑室内（ICV）注射促肾上腺皮质激素释放因子（CRF）拮抗剂（α-螺旋CRF9-41，30微克）可显著减弱IL-1β诱导的去甲肾上腺素释放增加。ICV注射CRF（2微克）也可导致脾脏去甲肾上腺素显著增加，分别在20分钟和140分钟出现两个明显的峰值。这些结果表明，腹腔注射IL-1β通过激活交感神经促进脾脏中去甲肾上腺素的释放，而交感神经活动的增加至少部分是由于大脑中含CRF的神经元兴奋所致。
