Andén N E, Grabowska-Andén M, Liljenberg B
J Neural Transm. 1983;58(3-4):143-52. doi: 10.1007/BF01252801.
Following interruption of the nerve impulse flow in the dopamine neurons by treatment with gammabutyrolactone, the selective dopamine autoreceptor agonist B-HT 920 reduced the DOPA accumulation after DOPA decarboxylase inhibition and the 3,4-dihydroxyphenylacetic acid concentration in the corpus striatum, the nucleus accumbens, the olfactory tubercle, the limbic cortex and the rostral part of the cerebral cortex of rats. The effects were completely inhibited by the dopamine receptor antagonist haloperidol, indicating that they were caused by stimulation of dopamine autoreceptors. In the caudal part of the cerebral cortex and the cerebellum, B-HT 920 somewhat reduced the concentration of dihydroxyphenylacetic acid via a haloperidol-sensitive mechanism, suggesting that there are a few dopamine neurons with autoreceptors in these regions. No evidence was obtained for the presence of autoreceptors on the dopamine neurons in the hypothalamus. The gammabutyrolactone-induced elevation of the dopamine concentration was not reduced by B-HT 920 in any region, suggesting that this effect of gammabutyrolactone was caused by decreased release rather than increased synthesis of dopamine under our experimental circumstances.
在用γ-丁内酯处理使多巴胺神经元中的神经冲动传导中断后，选择性多巴胺自身受体激动剂B-HT 920降低了多巴脱羧酶抑制后多巴的蓄积以及大鼠纹状体、伏隔核、嗅结节、边缘皮质和大脑皮质前部中3,4-二羟基苯乙酸的浓度。这些作用被多巴胺受体拮抗剂氟哌啶醇完全抑制，表明它们是由多巴胺自身受体的刺激引起的。在大脑皮质后部和小脑中，B-HT 920通过氟哌啶醇敏感机制略微降低了二羟基苯乙酸的浓度，提示在这些区域存在少数带有自身受体的多巴胺神经元。未获得下丘脑多巴胺神经元上存在自身受体的证据。在任何区域，B-HT 920均未降低γ-丁内酯诱导的多巴胺浓度升高，提示在我们的实验条件下，γ-丁内酯的这种作用是由多巴胺释放减少而非合成增加所致。
