Piazza P V, Rougé-Pont F, Deroche V, Maccari S, Simon H, Le Moal M
Laboratoire de Psychobiologie des Comportements Adaptatifs, Institut National de la Santé et de la Recherche Médical Unité 259. Université de Bordeaux II, France.
Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8716-20. doi: 10.1073/pnas.93.16.8716.
An increase in the activity of mesencephalic dopaminergic neurons has been implicated in the appearance of pathological behaviors such as psychosis and drug abuse. Several observations suggest that glucocorticoids might contribute to such an increase in dopaminergic activity. The present experiments therefore analyzed the effects of corticosterone, the major glucocorticoid in the rat, both on dopamine release in the nucleus accumbens of freely moving animals by means of microdialysis, and on locomotor activity, a behavior dependent on accumbens dopamine. Given that glucocorticoids have certain state-dependent neuronal effects, their action on dopamine was studied in situations differing in dopaminergic tonus, including during the light and dark phases of the circadian cycle, during eating, and in groups of animals differing in their locomotor reactivity to novelty. Dopaminergic activity is increased in the dark period, further increased during food-intake, and is higher in rats defined as high responders to novelty than in low responders. Corticosterone, peripherally administered in a dose that approximates stress-induced plasma concentrations, increased extracellular concentrations of dopamine, and this increase was augmented in the dark phase, during eating, and in high responder rats. Corticosterone had little or no effects in the light phase and in low responder rats. Corticosterone also stimulated locomotor activity, an effect that paralleled the release of dopamine and was abolished by neurochemical (6-hydroxydopamine) depletion of accumbens dopamine. In conclusion, glucocorticoids have state-dependent stimulant effects on mesencephalic dopaminergic transmission, and an interaction between these two factors might be involved in the appearance of behavioral disturbances.
中脑多巴胺能神经元活动的增加与诸如精神病和药物滥用等病理行为的出现有关。一些观察结果表明,糖皮质激素可能导致多巴胺能活动的这种增加。因此,本实验分析了大鼠体内主要的糖皮质激素皮质酮,对自由活动动物伏隔核中多巴胺释放的影响(通过微透析法),以及对运动活动的影响(一种依赖于伏隔核多巴胺的行为)。鉴于糖皮质激素具有某些状态依赖性的神经元效应,我们在多巴胺能张力不同的情况下研究了它们对多巴胺的作用,包括在昼夜节律周期的明相和暗相期间、进食期间,以及对新奇事物运动反应性不同的动物组中。多巴胺能活动在黑暗期增加,在进食期间进一步增加,并且在被定义为对新奇事物高反应者的大鼠中比低反应者更高。以接近应激诱导血浆浓度的剂量外周给予皮质酮,会增加多巴胺的细胞外浓度,并且这种增加在暗相、进食期间以及高反应者大鼠中会增强。皮质酮在明相和低反应者大鼠中几乎没有影响。皮质酮还刺激运动活动,这种效应与多巴胺的释放平行,并且通过伏隔核多巴胺的神经化学(6-羟基多巴胺)耗竭而被消除。总之,糖皮质激素对中脑多巴胺能传递具有状态依赖性的刺激作用,这两个因素之间的相互作用可能与行为障碍的出现有关。