Andén N E, Grabowska-Andén M, Liljenberg B
J Neural Transm. 1983;57(3):129-37. doi: 10.1007/BF01245113.
The alpha-methyltyrosine-induced disappearance of dopamine was inhibited by the selective dopamine autoreceptor agonist B-HT 920 in the corpus striatum, the nucleus accumbens, the olfactory tubercle, the limbic cortex, and the rostral part of the cerebral cortex of the rat. These inhibitory actions of B-HT 920 were almost completely reversed by the dopamine receptor antagonist haloperidol, indicating that they were caused by a stimulation of dopamine autoreceptors. In the caudal cortex and the cerebellum, the effects of B-HT 920 and haloperidol were less clear, perhaps due to a low concentration of dopamine and to the occurrence of this dopamine in both dopamine and noradrenaline neurons. In the hypothalamus, B-HT 920 and haloperidol did not change the alpha-methyltyrosine-induced disappearance of dopamine in agreement with previous findings that the tubero-infundibular dopamine neurons are not regulated via dopamine receptors.
在大鼠的纹状体、伏隔核、嗅结节、边缘皮质和大脑皮质前部,选择性多巴胺自身受体激动剂B-HT 920抑制了α-甲基酪氨酸诱导的多巴胺消失。多巴胺受体拮抗剂氟哌啶醇几乎完全逆转了B-HT 920的这些抑制作用,表明它们是由多巴胺自身受体的刺激引起的。在尾状皮质和小脑中,B-HT 920和氟哌啶醇的作用不太明确,这可能是由于多巴胺浓度较低以及多巴胺在多巴胺能神经元和去甲肾上腺素能神经元中均有存在。在下丘脑中,B-HT 920和氟哌啶醇并未改变α-甲基酪氨酸诱导的多巴胺消失,这与之前关于结节漏斗多巴胺神经元不受多巴胺受体调节的研究结果一致。