Glass Michael J, Briggs Jacquie E, Billington Charles J, Kotz Catherine M, Levine Allen S
Weill Medical College, Cornell University, New York, NY 10021, USA.
Am J Physiol Regul Integr Comp Physiol. 2002 Jul;283(1):R161-7. doi: 10.1152/ajpregu.00480.2001.
It has been suggested that an opioidergic feeding pathway exists between the nucleus of the solitary tract (NTS) and the central nucleus of the amygdala. We studied the following three groups of rats: 1) artificial cerebrospinal fluid (CSF) infused in the NTS, 2) naltrexone (100 microg/day) infused for 13 days in the NTS, and 3) artificial CSF infused in the NTS of rats pair fed to the naltrexone-infused group. Naltrexone administration resulted in a decrease in body weight and food intake. Also, naltrexone infusion increased dynorphin, but not enkephalin, gene expression in the amygdala, independent of the naltrexone-induced reduction in food intake. Gene expression of neuropeptide Y in the arcuate nucleus and neuropeptide Y peptide levels in the paraventricular nucleus did not change because of naltrexone infusion. However, naltrexone induced an increase in serum leptin compared with pair-fed controls. Thus chronic administration of naltrexone in the NTS increased dynorphin gene expression in the amygdala, further supporting an opioidergic feeding pathway between these two brain sites.
有人提出，在孤束核（NTS）和杏仁核中央核之间存在一条阿片能进食通路。我们研究了以下三组大鼠：1）向NTS注入人工脑脊液（CSF）；2）向NTS注入纳曲酮（100微克/天），持续13天；3）向与注入纳曲酮组配对饲养的大鼠的NTS注入人工脑脊液。给予纳曲酮导致体重和食物摄入量下降。此外，注入纳曲酮增加了杏仁核中强啡肽而非脑啡肽的基因表达，这与纳曲酮引起的食物摄入量减少无关。由于注入纳曲酮，弓状核中神经肽Y的基因表达和室旁核中神经肽Y的肽水平没有变化。然而，与配对饲养的对照组相比，纳曲酮诱导血清瘦素增加。因此，在NTS中长期给予纳曲酮增加了杏仁核中强啡肽基因的表达，进一步支持了这两个脑区之间的阿片能进食通路。
