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毒蕈碱受体和烟碱受体对神经节乙酰胆碱释放的突触前调制。

Presynaptic modulation of ganglionic ACh release by muscarinic and nicotinic receptors.

作者信息

Dujic Z, Roerig D L, Schedewie H K, Kampine J P, Bosnjak Z J

机构信息

Department of Anesthesiology, Medical College of Wisconsin, Milwaukee.

出版信息

Am J Physiol. 1990 Aug;259(2 Pt 2):R288-93. doi: 10.1152/ajpregu.1990.259.2.R288.

Abstract

The present experiments were undertaken to investigate the effects of atropine and d-tubocurarine on acetylcholine (ACh) release and ganglionic synaptic transmission in the isolated cat stellate ganglion. Ganglionic release of picomole amounts of ACh was measured by radioenzymatic assay, and ganglionic transmission was estimated on the basis of the compound action potential recorded from the postganglionic stellate cardiac nerve. Atropine (5 microM) produced a significant increase in both spontaneous and evoked ACh release from the ganglion while depressing synaptic transmission. d-Tubocurarine (20 microM) also caused a significant, though smaller, increase in spontaneous release of ACh but had little effect on evoked release of ACh. These results suggest that ACh release and synaptic transmission in the cat stellate ganglion are subject to cholinergic feedback regulation, which appears to be mediated predominantly via muscarinic presynaptic receptors.

摘要

进行本实验是为了研究阿托品和d -筒箭毒碱对离体猫星状神经节中乙酰胆碱(ACh)释放和神经节突触传递的影响。通过放射酶法测定皮摩尔量ACh的神经节释放量,并根据从节后星状心神经记录的复合动作电位来评估神经节传递。阿托品(5微摩尔)使神经节中自发和诱发的ACh释放均显著增加,同时抑制突触传递。d -筒箭毒碱(20微摩尔)也使ACh的自发释放显著增加,尽管增加幅度较小,但对诱发的ACh释放几乎没有影响。这些结果表明,猫星状神经节中的ACh释放和突触传递受到胆碱能反馈调节,这种调节似乎主要通过毒蕈碱型突触前受体介导。

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