Embryonic motor activity and implications for regulating motoneuron axonal pathfinding in zebrafish.

Embryonic motor activity and implications for regulating motoneuron axonal pathfinding in zebrafish.
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DOI:
10.1111/j.1460-9568.2008.06418.x
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发表时间:
2008-09
期刊:
The European journal of neuroscience
影响因子:
--
通讯作者:
Svoboda KR
Svoboda KR
中科院分区:
其他
文献类型:
--
作者:
Menelaou E;Husbands EE;Pollet RG;Coutts CA;Ali DW;Svoboda KR

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斑马鱼胚胎在受精后18-19小时,从保护性绒毛膜中取出后,肌肉组织就能自发收缩。这些运动可能是由早期胚胎中枢神经系统活动启动的。我们已经观察到,思维狭窄的突变胚胎(以下简称nrd−/−)在脱绒后缺乏正常的胚胎运动输出。然而,这些突变体可以游泳,并在幼虫发育阶段对触觉刺激作出反应。nrd−/−胚胎表现出神经嵴发育缺陷,肌肉发育缓慢,并且缺乏脊髓机械感觉神经元(称为Rohon-Beard(RB)神经元)。在早期发育阶段(即21-22 hpf),而仍然在他们的绒毛膜,nrd兄弟姐妹(nrd+/?)表现出肌肉组织收缩的速率与野生型胚胎相似。解剖学分析表明,RB神经元存在于运动胚胎中,但不存在于非运动胚胎中,表明非运动胚胎是nrd−/−胚胎。对nrd−/−胚胎的进一步解剖分析显示,运动神经元轴突寻路的错误一直持续到发育的幼虫阶段。当nrd−/−胚胎从21 hpf开始在高[K+]中培养时,这些错误被逆转,表明异常轴突表型可能与发育早期缺乏去极化活性有关。当在野生型胚胎中用三卡因阻断活性时,运动神经元表型与nrd−/−胚胎中的运动神经元表型相似。这些结果暗示早期胚胎活动与其他因素的正常运动神经元发育所必需的。
Zebrafish embryos exhibit spontaneous contractions of the musculature as early as 18–19 h post fertilization (hpf) when removed from their protective chorion. These movements are likely initiated by early embryonic central nervous system activity. We have made the observation that narrowminded mutant embryos (hereafter, nrd−/−) lack normal embryonic motor output upon dechorionation. However, these mutants can swim and respond to tactile stimulation by larval stages of development. nrd−/− embryos exhibit defects in neural crest development, slow muscle development and also lack spinal mechanosensory neurons known as Rohon–Beard (RB) neurons. At early developmental stages (i.e. 21–22 hpf) and while still in their chorions, nrd siblings (nrd+/?) exhibited contractions of the musculature at a rate similar to wild-type embryos. Anatomical analysis indicated that RB neurons were present in the motile embryos, but absent in the non-motile embryos, indicating that the non-motile embryos were nrd−/− embryos. Further anatomical analysis of nrd−/− embryos revealed errors in motoneuron axonal pathfinding that persisted into the larval stage of development. These errors were reversed when nrd−/− embryos were raised in high [K+] beginning at 21 hpf, indicating that the abnormal axonal phenotypes may be related to a lack of depolarizing activity early in development. When activity was blocked with tricaine in wild-type embryos, motoneuron phenotypes were similar to the motoneuron phenotypes in nrd−/− embryos. These results implicate early embryonic activity in conjunction with other factors as necessary for normal motoneuron development.
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