Smagin G N, Howell L A, Ryan D H, De Souza E B, Harris R B
Pennington Biomedical Research Center, Lousiana State University, Baton Rouge 70808, USA.
Neuroreport. 1998 May 11;9(7):1601-6. doi: 10.1097/00001756-199805110-00063.
The experiments presented in this study were designed to assess corticotropin-releasing factor (CRF) receptor subtype mediation of CRF- and urocortin (UCN)-induced decrease in food intake. Male Sprague-Dawley rats were treated with antisense and sense oligonucleotides (ON) to CRF2 receptor mRNAs for 36 h and then received an intracerebroventricular (i.c.v.) injection of CRF, UCN (3 micrograms) or saline. Antisense treatment significantly attenuated CRF- and UCN-induced suppression in food intake and HPA activation. Administration of CRF1 receptor antagonist did not affect the decrease in food intake or activation of the HPA axis induced by i.c.v. infusion of 3 micrograms CRF. The data suggest that down-regulation of CRF2 receptors selectively attenuates CRF- and UCN-induced anorexia and hypothalamo-pituitary-adrenocortical activation in rats.
本研究中的实验旨在评估促肾上腺皮质激素释放因子（CRF）受体亚型对CRF和尿皮质素（UCN）诱导的食物摄入量减少的介导作用。将雄性Sprague-Dawley大鼠用针对CRF2受体mRNA的反义寡核苷酸和正义寡核苷酸处理36小时，然后进行脑室内（i.c.v.）注射CRF、UCN（3微克）或生理盐水。反义处理显著减弱了CRF和UCN诱导的食物摄入量抑制和HPA激活。给予CRF1受体拮抗剂并不影响脑室内注射3微克CRF所诱导的食物摄入量减少或HPA轴激活。数据表明，CRF2受体的下调选择性地减弱了大鼠中CRF和UCN诱导的厌食以及下丘脑-垂体-肾上腺皮质激活。
