mellitus (DM) and to investigate the regulation of ghrelin pathway between arcuate and septal nucleus nuclei on gastric mo -tility.METHODS:Streptozotocin was injected intraperitoneally to establish a DM rat model .Fluorescence immunohisto-chemistry and real-time PCR were used to detect the expression of ghrelin receptor GHS-R1a.The gastric motility was eval-uated by implantation of a force transducer on the surface of rats'stomachs and the motility index was also calculated .The neural connections between arcuate and septal nuclei were analyzed by the technique of fluorogold tracing .The neural con-trol pathway of gastric motility was determined by central drug injection , nucleus lesion or nucleus electrical stimulation . RESULTS:The expression of GHS-R1a in the septal nucleus of DM rats was lower than that in normal rats (P<0.05). The amplitude and frequency of gastric motility in the DM rats were lower than those in the normal rats (P<0.05).The gastric motility of normal and DM rats were increased by injection of ghrelin into the septal nucleus in a dose -dependent manner.Seven days after injection of fluorogold into the septal nucleus , some neurons in arcuate nucleus were labeled by fluorogold and part of the labeled neurons were ghrelin immunopositive .No effect of nucleus lesion or nucleus electrical stimulation on the gastric motility in the normal rats was observed .In DM rats, the lesion of septal nucleus decreased the gastric motility (P<0.05).In the normal rats, the change of gastric motility caused by electrical stimulation in arcuate nucleus was not affected by the lesion of septal nucleus (P>0.05), while the change was attenuated in DM rats (P<0.05).The ghrelin receptor antagonist [D-Lys-3]-GHRP-6 had no significant effect on the gastric motility induced by electrical stimulation in arcuate nucleus of the normal rats (P>0.05), but it reduced the change in the DM rats (P<0.05).CONCLUSION:Ghrelin in septal nucleus and the ghrelinergic pathway between arcuate and septal nuclei play an important role in the modulation of gastric motility in DM rats .%目的：研究隔核ghrelin对糖尿病（DM）大鼠胃运动的调控，并探讨下丘脑弓状核与隔核间ghrelin通路对胃运动的调控机制。方法：链脲佐霉素腹腔注射制备DM大鼠模型；荧光免疫组化和real-time PCR方法检测DM大鼠隔核内ghrelin受体GHS-R1a表达变化；大鼠胃表面固定感应片在体记录胃运动并计算胃运动变化率；荧光金逆行示踪方法显示下丘脑弓状核和隔核间纤维联系，并采用中枢注射药物、核团损毁或电刺激等方法观察核团纤维联系对DM大鼠胃运动的调控作用。结果：（1） DM大鼠隔核GHS-R1a表达低于正常大鼠（P＜0.05），胃运动明显减弱，胃收缩幅度和频率显著降低（P＜0．05）。（2）隔核注射ghrelin增强正常和DM大鼠胃运动（P＜0.05），且呈量效关系。（3）荧光金在注射入隔核7 d后逆行至弓状核内神经元，其中部分神经元为ghrelin免疫阳性神经元；（4）正常大鼠体内，损毁隔核对胃运动和电刺激弓状核引起的胃运动变化无显著影响（P＞0．05）；而对DM大鼠，损毁隔核减弱胃运动和电刺激弓状核后胃运动（P＜0．05）。（5）隔核微量注射ghrelin受体阻断剂[D-Lys-3]-GHRP-6未显著改变正常大鼠电刺激弓状核后胃运动变化（P＞0．05），但可减弱DM大鼠电刺激弓状核引起的胃运动变化（P＜0．05）。结论：隔核ghrelin和下丘脑弓状核-隔核间ghrelin通路在糖尿病大鼠胃运动调控中发挥重要作用。
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