Rowland N, Stricker E M
Physiol Behav. 1982 Feb;28(2):271-7. doi: 10.1016/0031-9384(82)90074-9.
Dopamine (DA)-depleting brain lesions of various sizes were produced in rats either by intracerebroventricular injections of 6-hydroxydopamine (6-HDA) or by electrolytic lesions of the lateral hypothalamic (LH) area. Among 30 animals that became aphagic and adipsic for at least four days after large LH or 6-HDA-induced brain lesions, only three developed hyperphagia after electrolytic lesions of the ventromedial hypothalamus (VMH) or daily injections of long-acting protamine-zinc insulin (PZI). In 20 rats with smaller LH or 6-HDA-induced lesions, which had not shown marked initial behavioral dysfunctions, only three gained as much weight after VMH lesions as the control animals. Similarly, 6 of 10 rats with smaller LH lesions could not tolerate a 15-day series of PZI treatments, although 14 of 17 rats with smaller 6-HDA-induced lesions increased their food intake and gained weight during the PZI treatments as did control animals. These results indicate that hypothalamic hyperphagia can be blocked by DA-depleting brain lesions that neither produce an initial period of aphagia and adipsia nor involve hypothalamic tissue. They further indicate that even small LH lesions may prevent the development of hyperphagia elicited by PZI, whereas only very large 6-HDA-induced lesions consistently have this effect.
通过脑室内注射6-羟基多巴胺（6-HDA）或下丘脑外侧（LH）区的电解损伤，在大鼠中制造了各种大小的多巴胺（DA）耗竭性脑损伤。在30只动物中，在大的LH或6-HDA诱导的脑损伤后至少四天出现拒食和拒饮，只有三只在腹内侧下丘脑（VMH）电解损伤或每日注射长效鱼精蛋白锌胰岛素（PZI）后出现食欲亢进。在20只患有较小LH或6-HDA诱导损伤的大鼠中，这些大鼠最初没有表现出明显的行为功能障碍，只有三只在VMH损伤后体重增加与对照动物一样多。同样，10只患有较小LH损伤的大鼠中有6只不能耐受为期15天的PZI治疗系列，尽管17只患有较小6-HDA诱导损伤的大鼠中有14只在PZI治疗期间食物摄入量增加且体重增加，与对照动物一样。这些结果表明，下丘脑性食欲亢进可被DA耗竭性脑损伤阻断，这些损伤既不产生初始的拒食和拒饮期，也不涉及下丘脑组织。它们进一步表明，即使是小的LH损伤也可能阻止由PZI引起的食欲亢进的发展，而只有非常大的6-HDA诱导损伤始终具有这种作用。
