Levine A S, Grace M, Billington C J
Neuroendocrine Research Laboratory, U.S. Department of Veterans Affairs Medical Center, Minneapolis, MN 55417.
Brain Res. 1991 Oct 25;562(2):281-4. doi: 10.1016/0006-8993(91)90632-6.
We studied the effect of the mu antagonist, beta-funaltrexamine (beta-FNA) on deprivation and opioid-induced feeding. Intracerebroventricular pre-treatment of 20 h deprived rats with 0.1, 1, 10 and 20 nmol of beta-FNA decreased feeding by 24%, 50%, 50% and 38% during the first hour. Central administration of beta-FNA (0.1, 1 and 10 nmol) also decreased feeding induced by the mu opioid agonist, DAMGO by 57%, 60% and 71%. Feeding induced by the delta agonist, DSLET, was decreased by pre-treatment with beta-FNA; but only during the 1-2 h time points, a time when relatively little food was ingested. Intraventricular injection of beta-FNA failed to alter feeding stimulated by the kappa opioid agonist, U-50,488H. These data further substantiate a role for the opioid receptor in deprivation and opioid-induced feeding.
我们研究了μ拮抗剂β-氟纳曲胺(β-FNA)对饥饿和阿片类药物诱导进食的影响。对20小时未进食的大鼠进行脑室内预处理,给予0.1、1、10和20纳摩尔的β-FNA,在第一个小时内进食量分别减少了24%、50%、50%和38%。脑室内注射β-FNA(0.1、1和10纳摩尔)也使μ阿片类激动剂DAMGO诱导的进食量分别减少了57%、60%和71%。δ激动剂DSLET诱导的进食量在β-FNA预处理后减少,但仅在1 - 2小时这个进食相对较少的时间段内。脑室内注射β-FNA未能改变κ阿片类激动剂U - 50,488H刺激的进食。这些数据进一步证实了阿片受体在饥饿和阿片类药物诱导进食中的作用。