Leviel V, Gobert A, Guibert B
Laboratoire de Physiologie Nerveuse, Département de Neurophysiologie Appliquée, C.N.R.S., Gif sur Yvette, France.
Neuroscience. 1990;39(2):305-12. doi: 10.1016/0306-4522(90)90269-a.
A push-pull cannula supplied with an artificial cerebrospinal fluid containing the tritiated precursor of dopamine, [3H]tyrosine, was implanted in the caudate nucleus of rats anesthetized with halothane. The extracellular dopamine and dihydroxyphenylacetic acid were measured in successive 20 min fractions (both in their tritiated and unlabeled form) and the ratio between the two forms calculated. Glutamate was added to the superfusing cerebrospinal fluid to investigate its role in the process of dopamine release. The release of dopamine and the efflux of dihydroxyphenylacetic acid were activated by a low concentration (10(-8) M) of glutamate. In contrast, a higher concentration (10(-4) M) of the amino acid reduced the release of dopamine. These results first confirmed the presence of a dual mechanism of control, by glutamate, of the dopamine release in the striatum depending on the extracellular concentration. Secondly, these treatments affected the dihydroxyphenylacetic acid amount and predominantly the tritiated form of dopamine, suggesting that the glutamate induces an important increase of the amine synthesis, in spite of a moderate effect on the release. The reversal of the inhibition by applications of tetrodotoxin (5 x 10(-7) M) and bicuculline (10(-4) M) confirmed that it was mediated by an indirect mechanism involving a GABAergic neurotransmission. In addition, the increase of the spontaneous dopamine release during bicuculline application suggested the existence of a tonic mechanism of inhibition of dopamine release in the striatum. This was confirmed by the fact that local xylocaine-induced anesthesia of the sensory motor cortex increased the spontaneous release of dopamine in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)
将一根配备含多巴胺的氚标记前体[³H]酪氨酸的人工脑脊液的推拉式套管，植入用氟烷麻醉的大鼠尾状核中。连续20分钟的时间段内测量细胞外多巴胺和二羟基苯乙酸（包括其氚标记和未标记形式），并计算两种形式之间的比率。向灌注的脑脊液中添加谷氨酸，以研究其在多巴胺释放过程中的作用。低浓度（10⁻⁸M）的谷氨酸激活了多巴胺的释放和二羟基苯乙酸的流出。相反，较高浓度（10⁻⁴M）的该氨基酸减少了多巴胺的释放。这些结果首先证实了谷氨酸对纹状体中多巴胺释放的控制存在双重机制，这取决于细胞外浓度。其次，这些处理影响了二羟基苯乙酸的量，主要是多巴胺的氚标记形式，这表明尽管对释放有适度影响，但谷氨酸诱导了胺合成的显著增加。应用河豚毒素（5×10⁻⁷M）和荷包牡丹碱（10⁻⁴M）后抑制作用的逆转证实，这是由涉及GABA能神经传递的间接机制介导的。此外，应用荷包牡丹碱期间多巴胺自发释放的增加表明纹状体中存在抑制多巴胺释放的紧张性机制。感觉运动皮层局部利多卡因诱导的麻醉增加纹状体中多巴胺的自发释放这一事实证实了这一点。（摘要截短于250字）
