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首页> 外文期刊>The European Journal of Neuroscience >CB1 receptor-mediated control of the release of endocannabinoids (as assessed by microdialysis coupled with LC/MS) in the rat hypothalamus.
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CB1 receptor-mediated control of the release of endocannabinoids (as assessed by microdialysis coupled with LC/MS) in the rat hypothalamus.

机译：CB1受体介导的大鼠下丘脑内大麻素释放的控制（通过微透析结合LC / MS评估）。

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摘要

In the present study, we examined the occurrence and potential regulation of endocannabinoid release by cannabinoid CB1 receptors in the rat brain. To this end, we developed a highly sensitive (limit of sensitivity 30-300 amol) new analytical method, combining online brain microdialysis with solid-phase extraction-liquid chromatography-tandem mass spectrometry, which allowed the detection in real time of trace amounts of endocannabinoids in the extracellular fluid. In the hypothalamus, anandamide and 2-arachidonoyl-glycerol release was stimulated following depolarization via local administration of K(+), with or without addition of Ca(2+), or glutamate application. Inhibition of fatty acid amide hydrolase by systemic administration of intraperitoneal (i.p.) URB597 (0.5 mg/kg) induced an increase of anandamide, but not 2-arachidonoyl-glycerol, outflow. The CB1 receptor antagonist rimonabant (10 mg/kg i.p.) increased, whereas the CB1 agonist WIN55,212-2 (2.5 mg/kg i.p.) decreased, anandamide release. Interestingly, the same treatments induced opposite changes in 2-arachidonoyl-glycerol release. At a dose of 3 mg/kg i.p., which by itself did not affect endocannabinoid release, rimonabant fully antagonized the effect of WIN55,212-2 (2.5 mg/kg i.p.). Taken together, these results suggest that CB1 receptors are able to control the local release of endocannabinoids in the hypothalamus via a feedback mechanism and strengthen the view that anandamide and 2-arachidonoyl-glycerol have distinct physiological roles.
机译：在本研究中，我们检查了大麻素CB1受体在大鼠脑中释放大麻素的发生和潜在调控。为此，我们开发了一种高度灵敏（灵敏度极限为30-300 amol）的新分析方法，将在线脑微透析与固相萃取-液相色谱-串联质谱相结合，可以实时检测痕量的细胞外液中的内源性大麻素。在下丘脑中，去极化后通过局部施用K（+），添加或不添加Ca（2+）或谷氨酸来刺激anandamide和2-arachidonoyl-甘油释放。通过全身性腹膜内（i.p.）URB597（0.5 mg / kg）抑制脂肪酸酰胺水解酶诱导了花生四烯酸酰胺的流出增加，但2-花生四烯酰基甘油没有被抑制。 CB1受体拮抗剂利莫那班（10 mg / kg i.p.）增加，而CB1激动剂WIN55,212-2（2.5 mg / kg i.p.）减少，anandamide释放。有趣的是，相同的处理引起2-花生四烯酰基-甘油释放的相反变化。以3 mg / kg i.p.的剂量本身不影响内源性大麻素的释放，利莫那班完全拮抗WIN55,212-2的作用（2.5 mg / kg i.p.）。综上所述，这些结果表明，CB1受体能够通过反馈机制控制下丘脑中内源性大麻素的局部释放，并进一步增强了对花生四烯酸和2-花生四烯酸甘油具有独特生理作用的观点。

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