Leibowitz S F, Rossakis C
Psychopharmacology (Berl). 1979 Mar 28;61(3):273-80. doi: 10.1007/BF00432272.
Injection of L-Dopa (0.8--200 nmoles) into the perifornical hypothalamus produced a dose-dependent suppression of feeding in hungry rats. This effect was positively correlated in magnitude with the same effect produced by the catecholamine agonists dopamine and epinephrine, and by the catecholamine-releasing drug amphetamine. L-Dopa's action was partially antagonized by separate injections of the dopaminergic blocker haloperidol (58% blockade) and the beta-adrenergic blocker propranolol (38% blockade). Combined injections of these two antagonists produced a 90% blockade of L-Dopa's effect. Perifornical administration of the dopa decarboxylase inhibitors Ro 4-4602 and MK-486 was also shown to reverse L-Dopas feeding suppression, at doses that enhanced the effect of injected dopamine and epinephrine. On the basis of these findings, L-Dopa appears to suppress food consumption in part through increased catecholamine synthesis, specifically within dopaminergic and adrenergic neurons of the perifornical hypothalamic region.
向饥饿大鼠的穹窿周下丘脑注射左旋多巴(0.8 - 200纳摩尔)可产生剂量依赖性的进食抑制作用。这种效应在强度上与儿茶酚胺激动剂多巴胺和肾上腺素以及儿茶酚胺释放药物苯丙胺所产生的相同效应呈正相关。单独注射多巴胺能阻滞剂氟哌啶醇(58%的阻断率)和β - 肾上腺素能阻滞剂普萘洛尔(38%的阻断率)可部分拮抗左旋多巴的作用。联合注射这两种拮抗剂可产生90%的左旋多巴效应阻断率。向穹窿周给予多巴脱羧酶抑制剂Ro 4 - 4602和MK - 486,在增强注射多巴胺和肾上腺素作用的剂量下,也显示可逆转左旋多巴对进食的抑制作用。基于这些发现,左旋多巴似乎部分通过增加儿茶酚胺合成来抑制食物消耗,特别是在穹窿周下丘脑区域的多巴胺能和肾上腺素能神经元内。