Neuromuscular development following tetrodotoxin-induced inactivity in mouse embryos.
Neuromuscular development following tetrodotoxin-induced inactivity in mouse embryos.
复制标题
河豚毒素诱导小鼠胚胎失活后的神经肌肉发育。
DOI：
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
F. Rieger
中科院分区：
文献类型：
--
作者：
L. Houenou;M. Pinçon;L. García;A. Harris;F. Rieger
采用生物化学和组织学方法研究了14 ~ 18天河豚毒素慢性宫内瘫痪小鼠胚胎神经肌肉系统的发育情况。失活胚胎中腰椎运动神经元（MNs）的数量高于对照组，表明运动神经元细胞死亡减少。随着MN数量的增加，脊髓和外周突触部位胆碱乙酰转移酶活性均显著升高。麻痹肌肉成熟肌纤维数量减少，核位于中心。肌酸激酶活性显著降低，每肌纤维总乙酰胆碱受体和受体簇数显著增加。类似的变化模式发生在突变小鼠肌肉发育不良（mdg）的神经肌肉系统中。然而，与mdg突变体相比，河豚毒素处理的肌肉在神经支配模式、兴奋-收缩耦合系统（即二联体和三联体）的超微结构方面以及二氢吡啶结合的程度上与对照相似。因此，神经肌肉不活动并不足以损害肌肉神经支配的模式或三联或二氢吡啶受体的外观。这些结果表明，肌肉发育不良中二氢吡啶结合位点和三联体的改变不能用不活动来解释，而必须反映一个更主要的缺陷，涉及调节肌肉分化的一个或多个方面的发育的结构基因。
Developmental aspects of the neuromuscular system in mouse embryos chronically paralyzed in utero with tetrodotoxin (TTX) between embryonic days 14 and 18 were studied using biochemical and histological methods. The number of lumbar spinal motoneurons (MNs) was higher in inactive embryos than in controls suggesting a decreased motoneuron cell death. In association with the increase in MN number, choline acetyltransferase activity was significantly increased in both spinal cord and peripheral synaptic sites. Paralyzed muscles exhibited a decreased number of mature myofibers and the nuclei were centrally located. Creatine kinase activity was greatly decreased and total acetylcholine receptor and receptor cluster numbers per myofiber were significantly increased in paralyzed muscles. A similar pattern of changes occurs in the neuromuscular system of the mutant mouse muscular dysgenesis (mdg). However, in contrast to the mdg mutant, tetrodotoxin-treated muscles were similar to controls in their innervation pattern, in the ultrastructural aspects of the excitation-contraction coupling system (i.e., dyads and triads) and in the extent of dihydropyridine binding. Thus, neuromuscular inactivity is not sufficient to impair the pattern of muscle innervation or the appearance of either the triadic junctions or dihydropyridine receptors. These results indicate that alterations of dihydropyridine binding sites and triads in muscular dysgenesis cannot be accounted for by inactivity but rather must reflect a more primary defect involving the structural gene(s) regulating the development of one or more aspects of muscle differentiation.
DOI：
10.1242/dev.107.2.331
发表时间：
1989
期刊：
Development (Cambridge, England)
影响因子：
--
作者：
Oppenheim,RW;Bursztajn,S;Prevette,D
通讯作者：
Prevette,D
通过靶标衍生的神经营养因子减少体内自然发生的运动神经元死亡。
DOI：
10.1126/science.3363373
发表时间：
1988
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Oppenheim,RW;Haverkamp,LJ;Prevette,D;McManaman,JL;Appel,SH
通讯作者：
Appel,SH
电不活动和去神经支配对发育中的大鼠肌肉中乙酰胆碱受体分布的影响。
影响因子：
2.7
作者：
Ziskind-Conhaim,L;Bennett,JI
通讯作者：
Bennett,JI