An α7 nicotinic and GABAB receptor-mediated pathway controls acetylcholine release in the tripartite neuromuscular junction

被引：1

作者：

Petrov, Konstantin ^{[1
,2
]}

Lenina, Oksana ^{[1
]}

Leroy, Jacqueline ^{[3
]}

Bernard, Veronique ^{[4
]}

Germain, Thibaut ^{[5
]}

Truong, Charles ^{[5
]}

Nurullin, Leniz ^{[2
,6
]}

Sibgatullina, Guzel ^{[2
]}

Ohno, Kinji ^{[7
]}

Samigullin, Dmitry ^{[2
,8
]}

Krejci, Eric ^{[3
]}

机构：

[1] RAS, FRC Kazan Sci Ctr, Arbuzov Inst Organ & Phys Chem, Kazan, Russia

[2] RAS, FRC Kazan Sci Ctr, Kazan Inst Biochem & Biophys, Kazan, Russia

[3] Univ Paris Cite, Ctr Borelli UMR 9010, CNRS, ENS Paris Saclay, Paris, France

[4] Sorbonne Univ, CNRS, INSERM, U1130,UMR 8246, Paris, France

[5] Univ Paris Saclay, Ctr Borelli UMR 9010, CNRS, ENS Paris Saclay, Gif Sur Yvette, France

[6] Kazan State Med Univ, Kazan, Russia

[7] Nagoya Univ Arts & Sci, Grad Sch Nutr Sci, Nisshin, Japan

[8] Kazan Natl Res Tech Univ, Dept Radiophoton & Microwave Technol, Kazan, Russia

来源：

JOURNAL OF PHYSIOLOGY-LONDON | 2024年

基金：

俄罗斯科学基金会;

关键词：

acetylcholine; acetylcholinesterase; aminobutyric acid; neuromuscular junction; CONGENITAL MYASTHENIC SYNDROME; COLQ; MICE; DEFICIENCY; MUSCLE; MOUSE; BUTYRYLCHOLINESTERASE; ELIMINATION; MUTATIONS; GENE;

D O I：

10.1113/JP287243

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Terminal Schwann cells (TSCs) are capable of regulating acetylcholine (ACh) release at the neuromuscular junction (NMJ). We have identified GABA as a gliotransmitter at mouse NMJs. When ACh activates alpha 7 nicotinic ACh receptor (nAChRs) on TSCs, GABA is released and activates GABA(B) receptors on the nerve terminal that subsequently reduce ACh release. Indeed, specific deletion of the alpha 7 nAChR in TSCs or inhibition of the metabotropic GABAB receptor prevents the reduction in the quantal content of the end-plate potential induced by cholinesterase inhibitors. The alpha 7/GABAB receptor-mediated pathway is activated when ACh that escapes from collagen Q (ColQ) anchored AChE in the synaptic cleft and from PRiMA-anchored butyrylcholinesterase on the TSC activates alpha 7 nAChRs on the TSC. Consequently, prolonged tetanic stimulation of isolated muscle activates the alpha 7/GABAB receptor pathway, which reduces post-tetanic ACh release. When AChE levels are low in neonatal mice, the alpha 7/GABAB receptor-mediated pathway decreases ACh release and reduces ex vivo muscle fatigue. For ColQ-deficient mice where AChE is not clustered, the decrease in A.h release following activation of this pathway contributes to mouse fatigue in vivo.

引用

页码：507 / 527

页数：21

共 52 条

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