Muscle and motor-skill dysfunction in a K+ channel-deficient mouse are not due to altered muscle excitability or fiber type but depend on the genetic background.

Muscle and motor-skill dysfunction in a K+ channel-deficient mouse are not due to altered muscle excitability or fiber type but depend on the genetic background.
复制标题

K 通道缺陷小鼠的肌肉和运动技能功能障碍不是由于肌肉兴奋性或纤维类型改变所致,而是取决于遗传背景。

DOI:
10.1007/s004240000248
复制
发表时间:
2000
期刊:
Pflugers Archiv : European journal of physiology
影响因子:
--
通讯作者:
Joho,RH
Joho,RH
中科院分区:
--
文献类型:
--
作者:
Sánchez,JA;Ho,CS;Vaughan,DM;Garcia,MC;Grange,RW;Joho,RH

文献摘要

相似文献

电压门控K+通道Kv3.1在骨骼肌和中枢神经系统的GABA能中间神经元中表达。因此,Kv3.1 K+通道的缺乏可能导致肌源性或神经源性起源的表型,或两者兼而有之。Kv3.1缺陷型(Kv3.1-/-)129/Sv小鼠显示其骨骼肌的收缩特性改变,并且在旋转杆上表现不佳。相比之下,(129/Sv × C57BL/6)F1背景下的Kv3.1-/-小鼠显示出正常的肌肉特性,表现与野生型小鼠相似。旋转杆上的不良表现与改变的肌肉特性的相关性支持Kv3.1-/-129/Sv小鼠中的骨骼肌功能障碍可能是旋转杆上的运动技能受损的原因。令人惊讶的是,我们没有发现野生型和Kv3.1-/-129/Sv骨骼肌之间在静息电位或动作电位、延迟整流钾电导(gK)或快肌和慢肌纤维分布方面的重大差异。这些研究结果表明,Kv3.1钾离子通道可能不会发挥主要作用,在骨骼肌纤维的内在兴奋性,虽然它的缺乏导致收缩和舒张较慢,并在129/Sv Kv3.1-/-小鼠肌肉较小的力量。
The voltage-gated K+channel Kv3.1 is expressed in skeletal muscle and in GABAergic interneurons in the central nervous system. Hence, the absence of Kv3.1 K+channels may lead to a phenotype of myogenic or neurogenic origin, or both. Kv3.1-deficient (Kv3.1–/–) 129/Sv mice display altered contractile properties of their skeletal muscles and show poor performance on a rotating rod. In contrast, Kv3.1–/–mice on the (129/Sv×C57BL/6)F1 background display normal muscle properties and perform like wild-type mice. The correlation of poor performance on the rotating rod with altered muscle properties supports the notion that the skeletal muscle dysfunction in Kv3.1–/–129/Sv mice may be responsible for the impaired motor skills on the rotating rod. Surprisingly, we did not find major differences between wild-type and Kv3.1–/–129/Sv skeletal muscles in either the resting or action potential, the delayed-rectifier potassium conductance (gK) or the distribution of fast and slow muscle fibers. These findings suggest that the Kv3.1 K+channel may not play a major role in the intrinsic excitability of skeletal muscle fibers although its absence leads to slower contraction and relaxation and to smaller forces in muscles of 129/Sv Kv3.1–/–mice.