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小鼠骨骼肌内向整流器的产后诱导及神经调节

Postnatal induction and neural regulation of inward rectifiers in mouse skeletal muscle.

作者信息

Gonoi T, Hasegawa S

机构信息

Research Centre for Pathogenic Fungi and Microbial Toxicoses, Chiba University, Japan.

出版信息

Pflugers Arch. 1991 Jul;418(6):601-7. doi: 10.1007/BF00370577.

DOI:10.1007/BF00370577
PMID:1719474
Abstract

The whole-cell voltage-clamp technique was used to examine developmental changes of inward rectifier currents in fibres of the flexor digitorum brevis muscle acutely isolated from mice on postnatal day 0 (P0) to P36. Neither a steady-state component (Is-s) nor a slowly activated component (Irise) of inward rectifier currents were observed in fibres of P0 and P4 mice. Both Is-s and Irise became apparent between days P8 and P16. The specific amplitudes of Is-s and Irise measured at a test-pulse potential of -100 mV at 20 mM extracellular K+ [( K+]o) increased to their respective platcau values of -68 +/- 10 and -15 +/- 7 microA/cm2 at P20. In fibres denervated on day P4 the developmental increase of Is-s was suppressed, its specific amplitude at P20 being one-tenth of that in the corresponding normal fibres. Irise did not appear in P4-denervated fibres throughout the development. In muscle fibres denervated at P16 or P20, the specific amplitudes of Is-s and Irise decreased, reaching the levels of P4-denervated fibres in 2-4 days after denervation. We conclude that Is-s and Irise develop within 3 weeks after birth, and suggest that innervation plays a key role in their induction.

摘要

采用全细胞膜片钳技术,研究了从出生后第0天(P0)至第36天的小鼠急性分离的趾短屈肌纤维内向整流电流的发育变化。在P0和P4小鼠的纤维中,未观察到内向整流电流的稳态成分(Is-s)和缓慢激活成分(Irise)。Is-s和Irise在P8至P16天之间变得明显。在20 mM细胞外钾离子浓度([K+]o)下,在-100 mV的测试脉冲电位下测量的Is-s和Irise的特定幅度在P20时分别增加到各自的平台值-68±10和-15±7 μA/cm2。在P4天去神经的纤维中,Is-s的发育增加受到抑制,其在P20时的特定幅度是相应正常纤维的十分之一。在整个发育过程中,Irise未出现在P4去神经的纤维中。在P16或P20天去神经的肌肉纤维中,Is-s和Irise的特定幅度降低,在去神经后2-4天达到P4去神经纤维的水平。我们得出结论,Is-s和Irise在出生后3周内发育,并表明神经支配在其诱导中起关键作用。

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Human myoblast fusion requires expression of functional inward rectifier Kir2.1 channels.人类成肌细胞融合需要功能性内向整流钾通道Kir2.1的表达。
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Induction of inward rectifiers in mouse skeletal muscle fibres in culture.

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