Angel I, Stivers J A, Paul S M, Crawley J N
Pharmacol Biochem Behav. 1987 Jun;27(2):291-7. doi: 10.1016/0091-3057(87)90572-7.
Feeding induced by 2-deoxyglucose was compared with feeding induced by food deprivation in terms of antagonism by anorectic drugs and of anatomical site of action. Glucoprivic feeding was completely blocked by microinjection of amphetamine, fenfluramine, and mazindol into the paraventricular nucleus of the hypothalamus (PVN). Deprivation-induced feeding was not blocked by amphetamine, fenfluramine, or mazindol microinjected into the PVN. Neither the feeding induced by 2-deoxyglucose nor its reversal by amphetamine were blocked by pretreatment with the beta-adrenergic antagonist, propranolol. Amphetamine and fenfluramine blocked both glucoprivic- and deprivation-induced feeding when microinjected into the perifornical region of the lateral hypothalamus. These data suggest that food consumption induced by 2-deoxyglucose treatment can be antagonized by anorectic drugs acting at recognition sites present in several hypothalamic nuclei, while deprivation-induced feeding acts through different receptor mechanisms which may be specific to the perifornical region of the lateral hypothalamus.
就厌食药物的拮抗作用和作用的解剖学部位而言，对2-脱氧葡萄糖诱导的进食与食物剥夺诱导的进食进行了比较。通过向下丘脑室旁核（PVN）微量注射苯丙胺、芬氟拉明和马吲哚，糖缺乏性进食被完全阻断。向PVN微量注射苯丙胺、芬氟拉明或马吲哚，剥夺诱导的进食未被阻断。用β-肾上腺素能拮抗剂普萘洛尔预处理，既不阻断2-脱氧葡萄糖诱导的进食，也不阻断其由苯丙胺引起的逆转。当向外侧下丘脑穹窿周区微量注射时，苯丙胺和芬氟拉明阻断糖缺乏性和剥夺诱导的进食。这些数据表明，2-脱氧葡萄糖处理诱导的食物消耗可被作用于几个下丘脑核中存在的识别位点的厌食药物拮抗，而剥夺诱导的进食通过不同的受体机制起作用，这些机制可能是外侧下丘脑穹窿周区特有的。
