Angrist B, Ain M, Rotrosen J, Gershon S, Halpern F S, Sachar E J
J Neural Transm. 1979;44(4):249-62. doi: 10.1007/BF01250321.
Low doses of the dopamine agonist ET-495 were administered to nonpsychotic volunteer subjects by slow intravenous infusion, followed by a bolus of 1.5--2.5 mg haloperidol. ET-495 caused progressive dysphoria and sedation (in some cases, light sleep), effects believed to be mediated by dopaminergic inhibition. However, ET-495 also elevated growth hormone and suppressed prolactin, typical responses to dopamine agonist activity. Haloperidol reversed both the sedation and prolactin suppression induced by ET-495. These findings suggest: (1) that the sedation and hormonal responses were produced by stimulation of dopamine receptors; (2) that neurotransmitter systems mediating behavioral and neuroendocrine regulation may have differential neuropharmacological characteristics.
通过缓慢静脉输注向非精神病志愿者受试者给予低剂量的多巴胺激动剂ET - 495，随后推注1.5 - 2.5毫克氟哌啶醇。ET - 495导致进行性烦躁不安和镇静（在某些情况下为浅睡眠），据信这些效应是由多巴胺能抑制介导的。然而，ET - 495还升高了生长激素并抑制了催乳素，这是对多巴胺激动剂活性的典型反应。氟哌啶醇逆转了ET - 495诱导的镇静和催乳素抑制。这些发现表明：（1）镇静和激素反应是由多巴胺受体刺激产生的；（2）介导行为和神经内分泌调节的神经递质系统可能具有不同的神经药理学特征。
