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α7 型烟碱型乙酰胆碱受体在青蛙神经肌肉接点中的突触传递作用。

Role of α7 Nicotinic Acetylcholine Receptors in Synaptic Transmission in Frog Neuromuscular Contacts.

机构信息

A. E. Arbuzov Institute of Organic and Physical Chemistry, Federal Research Center Kazan Scientific Center, Russian Academy of Sciences, Kazan, Republic of Tatarstan, Russia.

Kazan Institute of Biochemistry and Biophysics, Federal Research Center Kazan Scientific Center, Russian Academy of Sciences, Kazan, Republic of Tatarstan, Russia.

出版信息

Bull Exp Biol Med. 2022 Mar;172(5):534-538. doi: 10.1007/s10517-022-05427-0. Epub 2022 Mar 29.

DOI:10.1007/s10517-022-05427-0
PMID:35348952
Abstract

The role of α7 nicotinic acetylcholine receptors in coupling of synaptic activity and muscle contractions was studied in frog (Rana ridibunda) neuromuscular synapses. The amplitude of endplate currents, the probability of action potential generation, and the strength of muscle contractions decreased in the presence of selective α7 antagonist methyllycaconitine. The effects of nicotinic acetylcholine receptor blockade depended on the pattern of the motor nerve stimulation. It can be assumed that the muscle action potential is a factor of retrograde control of neurosecretion, which modulates activity of α7 nicotinic receptors and the release of acetylcholine from motor nerve endings.

摘要

α7 型烟碱型乙酰胆碱受体在突触活动和肌肉收缩偶联中的作用在青蛙(Rana ridibunda)的神经肌肉突触中进行了研究。在选择性 α7 拮抗剂甲基戊二酰胆碱存在的情况下,终板电流幅度、动作电位发生的概率和肌肉收缩的强度降低。烟碱型乙酰胆碱受体阻断的作用取决于运动神经刺激的模式。可以假设肌肉动作电位是神经分泌逆行控制的一个因素,它调节α7 型烟碱受体的活性和运动神经末梢乙酰胆碱的释放。

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本文引用的文献

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A Novel Striated Muscle-Specific Myosin-Blocking Drug for the Study of Neuromuscular Physiology.一种用于神经肌肉生理学研究的新型横纹肌特异性肌球蛋白阻断药物。
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A novel synaptic plasticity rule explains homeostasis of neuromuscular transmission.一种新的突触可塑性规则解释了神经肌肉传递的稳态。
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Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesicles Underlies Rapid Homeostatic Plasticity of Quantal Content.
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Schwann cells sense and control acetylcholine spillover at the neuromuscular junction by α7 nicotinic receptors and butyrylcholinesterase.施万细胞通过α7 烟碱型乙酰胆碱受体和丁酰胆碱酯酶感知和控制神经肌肉接头处的乙酰胆碱溢出。
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Reactive oxygen species inactivate neuronal nicotinic acetylcholine receptors through a highly conserved cysteine near the intracellular mouth of the channel: implications for diseases that involve oxidative stress.活性氧通过位于通道细胞内口附近高度保守的半胱氨酸使神经元烟碱型乙酰胆碱受体失活:涉及氧化应激的疾病的影响。
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Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system.神经系统中烟碱型乙酰胆碱受体介导的钙信号传导
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Mitochondrial reactive oxygen species inactivate neuronal nicotinic acetylcholine receptors and induce long-term depression of fast nicotinic synaptic transmission.线粒体活性氧使神经元烟碱型乙酰胆碱受体失活,并诱导快速烟碱型突触传递的长期抑制。
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Transsynaptic modulation of the synaptic vesicle cycle by cell-adhesion molecules.细胞粘附分子对突触小泡循环的跨突触调节
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Rapid activation of presynaptic nicotinic acetylcholine receptors by nerve-released transmitter.神经释放的递质对突触前烟碱型乙酰胆碱受体的快速激活。
Eur J Neurosci. 2003 Dec;18(11):2946-56. doi: 10.1111/j.1460-9568.2003.03064.x.