Napier T C, Pirch J H, Strahlendorf H K
Neuroscience. 1983 May;9(1):53-9. doi: 10.1016/0306-4522(83)90046-5.
This study was designed to examine the ability of naloxone to antagonize the inhibition of neurons in the globus pallidus produced by electrical stimulation of the caudate nucleus. In rats anesthetized with chloral hydrate, bipolar stimulating electrodes were placed in the head of the caudate and seven-barrel micropipettes were utilized for recording extracellular activity of globus pallidus cells as well as for microiontophoretic application of experimental drugs. In most globus pallidus cells which were inhibited by caudate stimulation, application of naloxone (at currents which antagonized morphine-elicited depression) attenuated the caudate-induced effect. Naloxone did not antagonize depression of globus pallidus neurons induced by gamma-aminobutyrate. The results indicate that caudate stimulation causes the release of endogenous enkephalins which act to suppress neuronal activity in the globus pallidus. Thus, this study supports biochemical and histochemical studies which provide evidence for an enkephalinergic component in the striatopallidal projection.
本研究旨在检测纳洛酮拮抗由电刺激尾状核所引起的苍白球神经元抑制作用的能力。在用氯醛水合物麻醉的大鼠中,将双极刺激电极置于尾状核头部,并使用七管微量移液器记录苍白球细胞的细胞外活动以及用于实验药物的微量离子导入。在大多数受尾状核刺激抑制的苍白球细胞中,应用纳洛酮(在拮抗吗啡引起的抑制作用的电流下)可减弱尾状核诱导的效应。纳洛酮不能拮抗由γ-氨基丁酸引起的苍白球神经元的抑制作用。结果表明,尾状核刺激导致内源性脑啡肽的释放,其作用是抑制苍白球中的神经元活动。因此,本研究支持了生化和组织化学研究,这些研究为纹状体苍白球投射中的脑啡肽能成分提供了证据。