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鳗鱼中儿茶酚胺释放的胆碱能控制

Cholinergic control of catecholamine release in the eel.

作者信息

Al-Kharrat H, Weiss U, Tran Q, Nibbio B, Scholz S, Epple A

机构信息

Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

出版信息

Gen Comp Endocrinol. 1997 Oct;108(1):102-8. doi: 10.1006/gcen.1997.6954.

Abstract

The perifused posterior cardinal vein of the American eel (Anguilla rostrata) releases spontaneously dopamine (DA), norepinephrine (NE), and epinephrine (E). NE and E are secreted by innervated chromaffin cells, while DA is most likely released from a component of the vascular wall. Stimulation with acetylcholine strongly enhances the release of DA and E, and to a lesser degree the release of NE. Nicotine stimulates the release of all three catecholamines. Muscarine reduces the basal release of NE. Muscarine does not prevent nicotinic stimulation of NE and E release, but abolishes the nicotine effect on DA release. The muscarinic antagonist atropine stimulates the release of NE, but not of DA and E. The beta-adrenergic receptor antagonist propranolol suppresses the acetylcholine-stimulated release of NE and E, and reduces the DA response. From these findings, it appears that (1) nicotinic receptors regulate NE and E secretion from the chromaffin cells, (2) muscarinic receptors inhibit basal NE release, and (3) acetylcholine-stimulated release of NE and E requires the interaction with adrenergic receptors. On the other hand, DA release involves both nicotinic and adrenergic receptors, while the reduction of nicotine-stimulated (but not basal) DA release involves muscarinic receptors.

摘要

美洲鳗鲡(Anguilla rostrata)经灌流的后主静脉会自发释放多巴胺(DA)、去甲肾上腺素(NE)和肾上腺素(E)。NE和E由受神经支配的嗜铬细胞分泌,而DA很可能从血管壁的某一成分释放。乙酰胆碱刺激可强烈增强DA和E的释放,对NE释放的增强程度较小。尼古丁刺激所有三种儿茶酚胺的释放。毒蕈碱可降低NE的基础释放。毒蕈碱并不阻止尼古丁对NE和E释放的刺激作用,但可消除尼古丁对DA释放的影响。毒蕈碱拮抗剂阿托品刺激NE的释放,但不刺激DA和E的释放。β-肾上腺素能受体拮抗剂普萘洛尔可抑制乙酰胆碱刺激的NE和E释放,并降低DA反应。从这些发现来看,似乎(1)烟碱受体调节嗜铬细胞中NE和E的分泌,(2)毒蕈碱受体抑制NE的基础释放,(3)乙酰胆碱刺激的NE和E释放需要与肾上腺素能受体相互作用。另一方面,DA释放涉及烟碱受体和肾上腺素能受体,而尼古丁刺激的(而非基础的)DA释放的减少涉及毒蕈碱受体。

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