Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b.
Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b.
复制标题
斑马鱼的触摸反应需要电压门控钙通道 2.1b。
DOI：
10.1152/jn.00839.2011
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发表时间：
2012
影响因子：
2.5
通讯作者：
Saint-Amant,Louis
中科院分区：
文献类型：
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作者：
Low,SeanE;Woods,IanG;Lachance,Mathieu;Ryan,Joel;Schier,AlexanderF;Saint-Amant,Louis
对触摸不敏感的斑马鱼变异体的分子和生理基础仍然难以捉摸。在这里，我们报告了这种表型是由编码电压门控钙通道2.1b(CACNA1Ab)基因的错义突变引起的。注射编码野生型CaV2.1的RNA可以恢复FAKIR突变体的触摸反应，而敲除CACNA1 Abvia吗啉寡核苷酸则重现FAKIR突变体的表型。Fakir变异体在神经肌肉接头显示正常的电流诱发突触通讯，但减弱了触觉诱发的运动神经元激活。NMDA诱导的虚构游泳不受CaV2.1b丢失的影响，这表明该通道不是运动模式生成所必需的。这些结果，再加上CACNA1Abby感觉神经元的表达，表明CaV2.1b通道活动是触摸诱发的斑马鱼运动网络激活所必需的。
The molecular and physiological basis of the touch-unresponsive zebrafish mutantfakirhas remained elusive. Here we report that thefakirphenotype is caused by a missense mutation in the gene encoding voltage-gated calcium channel 2.1b (CACNA1Ab). Injection of RNA encoding wild-type CaV2.1 restores touch responsiveness infakirmutants, whereas knockdown ofCACNA1Abvia morpholino oligonucleotides recapitulates thefakirmutant phenotype.Fakirmutants display normal current-evoked synaptic communication at the neuromuscular junction but have attenuated touch-evoked activation of motor neurons. NMDA-evoked fictive swimming is not affected by the loss of CaV2.1b, suggesting that this channel is not required for motor pattern generation. These results, coupled with the expression ofCACNA1Abby sensory neurons, suggest that CaV2.1b channel activity is necessary for touch-evoked activation of the locomotor network in zebrafish.