Fukuda T, Tsumagari T
Nihon Yakurigaku Zasshi. 1984 Jun;83(6):485-96.
The effects of neuroleptic drugs on self-stimulation behavior were investigated in rats with electrodes chronically implanted in the lateral hypothalamus. Except for sulpiride and carpipramine, the neuroleptic drugs chlorpromazine, thioridazine, perphenazine, haloperidol, floropipamide, pimozide, clocapramine and oxypertine all suppressed self-stimulation behavior dose-dependently. The anti-anxiety drugs chlordiazepoxide, diazepam, clotiazepam and etizolam facilitated this behavior. The antidepressant drugs imipramine and amitriptyline suppressed this behavior slightly at the dose of 40 mg/kg. The alpha-antagonist phenoxybenzamine also suppressed this behavior, but the slope of its dose-response curve was gentle compared with those of the neuroleptic drugs. The inhibition produced by the neuroleptic drugs is considered to be mediated primarily at the dopaminergic receptors. Turning behavior induced by methamphetamine in rats with unilateral 6-hydroxydopamine lesions of the caudate nucleus was used to assess the striatal dopaminergic blocking potency of the neuroleptic drugs. No correlation was found between the ED50 values for the turning behavior inhibition and the ED50 values for the self-stimulation behavior inhibition produced by these drugs, so the dopaminergic receptors in the striatum are apparently not involved in the mediation of self-stimulation behavior.
将电极长期植入大鼠下丘脑外侧，研究了抗精神病药物对自我刺激行为的影响。除舒必利和卡比咪嗪外，抗精神病药物氯丙嗪、硫利达嗪、奋乃静、氟哌啶醇、氟罗哌丁酰胺、匹莫齐特、氯卡帕明和奥昔哌汀均剂量依赖性地抑制自我刺激行为。抗焦虑药物氯氮卓、地西泮、氯噻西泮和依替唑仑促进了这种行为。抗抑郁药物丙咪嗪和阿米替林在40mg/kg剂量时对这种行为有轻微抑制作用。α-拮抗剂酚苄明也抑制这种行为，但其剂量-反应曲线的斜率与抗精神病药物相比较为平缓。抗精神病药物产生的抑制作用主要被认为是通过多巴胺能受体介导的。用甲基苯丙胺诱导单侧6-羟基多巴胺损伤尾状核的大鼠产生旋转行为，以评估抗精神病药物的纹状体多巴胺能阻断效力。这些药物对旋转行为抑制的半数有效量（ED50）值与对自我刺激行为抑制的ED50值之间未发现相关性，因此纹状体中的多巴胺能受体显然不参与自我刺激行为的介导。
