Opioid receptor blockade in rat nucleus tractus solitarius alters amygdala dynorphin gene expression.
Academic Article
Overview
abstract
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.
