Fink J S, Smith G P
J Comp Physiol Psychol. 1979 Feb;93(1):66-73. doi: 10.1037/h0077583.
In a previous study rats were shown to have decreased locomotor and investigatory exploration after bilateral microinjections of 6-hydroxydopamine into the anterolateral hypothalamus. These deficits correlate with the loss of catecholamine terminals in neocortical, limbic, and anteromedioventral striatal brain sites. To test whether this correlation was causal, central catecholamines were increased by the intraperitoneal administration of L-3,4-dihydroxyphenylalanine (L-dopa), 10--40 mg/kg) after inhibition of extracerebral L-amino acid decarboxylase. Such treatment repaired the deficits in locomotor exploration and investigation in 6-hydroxydopamine rats. Pretreatment with the catecholamine antagonist chlorpromazine (1--2 mg/kg) blocked the increase in locomotor exploration and investigation produced by L-dopa in 6-hydroxydopamine rats. The results suggest, but do not prove, that L-dopa produced these behavioral effects by increasing central catecholamines at the denervated catecholamine receptor sites in the forebrain. These data and the data from the previous study are complementary evidence for the hypothesis that forebrain catecholamine synaptic action is necessary for normal exploratory behavior.
在先前的一项研究中，给大鼠双侧下丘脑前外侧微量注射6-羟基多巴胺后，其运动和探究性探索活动减少。这些缺陷与新皮质、边缘系统及前内侧腹侧纹状体脑区儿茶酚胺终末的丧失有关。为了检验这种相关性是否具有因果关系，在抑制脑外L-氨基酸脱羧酶后，腹腔注射L-3,4-二羟基苯丙氨酸（L-多巴，10 - 40mg/kg）来增加中枢儿茶酚胺。这样的处理修复了6-羟基多巴胺处理大鼠的运动探索和探究缺陷。用儿茶酚胺拮抗剂氯丙嗪（1 - 2mg/kg）预处理可阻断L-多巴对6-羟基多巴胺处理大鼠运动探索和探究活动的增加作用。结果提示（但未证实），L-多巴通过增加前脑去神经支配的儿茶酚胺受体部位的中枢儿茶酚胺而产生这些行为效应。这些数据以及先前研究的数据为下述假说提供了补充证据：前脑儿茶酚胺突触作用对正常的探索行为是必需的。
