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兰尼碱和肌醇三磷酸受体调节青蛙神经肌肉接头处的易化和强直后抑制。

Ryanodine and inositol triphosphate receptors modulate facilitation and tetanic depression at the frog neuromuscular junction.

作者信息

Silveira Priscila E, Lima Ricardo F, Guimarães Jennifer D S, Molgó Jordi, Naves Ligia A, Kushmerick Christopher

机构信息

Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antonio Carlos 6627, Belo Horizonte, Minas Gerais, 31270-901, Brazil.

Departamento Fisiologia e Farmacologia, UFC, Fortaleza, Brazil.

出版信息

Muscle Nerve. 2015 Oct;52(4):623-30. doi: 10.1002/mus.24571. Epub 2015 Jul 2.

DOI:10.1002/mus.24571
PMID:25600698
Abstract

INTRODUCTION

Short-term plasticity of synaptic function is an important physiological control of transmitter release. Short-term plasticity can be regulated by intracellular calcium released by ryanodine and inositol triphosphate (IP3) receptors, but the role of these receptors at the neuromuscular junction is understood incompletely.

METHODS

We measured short-term plasticity of evoked endplate potential (EPP) amplitudes from frog neuromuscular junctions treated with ryanodine, 2-aminoethoxydiphenylborane (2-APB), or 1-[6-[[(17β)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U- 73122).

RESULTS

Ryanodine decreases paired-pulse facilitation for intervals <20 ms and markedly decreases tetanic depression. Treatment with 2-APB reduces EPP amplitude, increases paired-pulse facilitation for intervals of <20 ms, and significantly reduces tetanic depression. U-73122 decreases EPP amplitude and decreases paired-pulse depression for intervals <20 ms.

CONCLUSIONS

Ryanodine, IP3 receptors, and phospholipase C modulate short-term plasticity of transmitter release at the neuromuscular junction. These results suggest possible targets for improving the safety factor of neuromuscular transmission during repetitive activity of the neuromuscular junction.

摘要

引言

突触功能的短期可塑性是递质释放的重要生理调控机制。短期可塑性可受由兰尼碱和三磷酸肌醇(IP3)受体释放的细胞内钙调节,但这些受体在神经肌肉接头处的作用尚未完全明确。

方法

我们测量了用兰尼碱、2-氨基乙氧基二苯硼(2-APB)或1-[6-[[(17β)-3-甲氧基雌甾-1,3,5(10)-三烯-17-基]氨基]己基]-1H-吡咯-2,5-二酮(U-73122)处理的青蛙神经肌肉接头诱发终板电位(EPP)幅度的短期可塑性。

结果

兰尼碱降低了间隔<20毫秒时的双脉冲易化,并显著降低强直后抑制。用2-APB处理可降低EPP幅度,增加间隔<20毫秒时的双脉冲易化,并显著降低强直后抑制。U-73122降低EPP幅度,并降低间隔<20毫秒时的双脉冲抑制。

结论

兰尼碱、IP3受体和磷脂酶C调节神经肌肉接头处递质释放的短期可塑性。这些结果提示了在神经肌肉接头重复活动期间改善神经肌肉传递安全系数的可能靶点。

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