Lopez-Valpuesta F J, Nyce J W, Myers R D
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858, USA.
Neuroreport. 1996 Nov 4;7(15-17):2781-4. doi: 10.1097/00001756-199611040-00075.
The central actions of neuropeptide Y antisense oligodeoxynucleotide (aNPY) and NPY-Y1 receptor antisense (aNPY-Y1) on body temperature (Tb), feeding and body weight of unrestrained rats were determined by the repeated intracerebroventricular (i.c.v.) injection of 0.5 microgram doses. aNPY-Y1 caused intense phasic rises in Tb, lowered body weight and caused transient feeding. aNPY increased food intake paradoxically, accompanied by a gain in body weight but did not affect Tb. Circadian activity was unaffected by either antisense oligodeoxynucleotide, and the mismatched NPY (mNPY) was without effect. These results show that NPY-Y1 receptors underlie the central thermolytic action of NPY, since aNPY-Y1 induces hyperthermic responses. Overall, the functional reduction in NPY activity by aNPY might cause a compensatory de novo synthesis of NPY in structures remote from the ventricles to augment feeding behavior.
通过反复脑室内（i.c.v.）注射0.5微克剂量，确定了神经肽Y反义寡脱氧核苷酸（aNPY）和NPY - Y1受体反义物（aNPY - Y1）对无拘束大鼠体温（Tb）、摄食和体重的中枢作用。aNPY - Y1引起Tb的强烈阶段性升高，降低体重并导致短暂摄食。aNPY反而增加食物摄入量，同时伴有体重增加，但不影响Tb。昼夜活动不受任何一种反义寡脱氧核苷酸的影响，错配的NPY（mNPY）也无作用。这些结果表明，NPY - Y1受体是NPY中枢产热作用的基础，因为aNPY - Y1诱导体温过高反应。总体而言，aNPY对NPY活性的功能降低可能导致在远离脑室的结构中重新合成NPY以增强摄食行为。
