Fibrillation and accelerated AChR degradation in long-term muscle organ culture.
Fibrillation and accelerated AChR degradation in long-term muscle organ culture.
复制标题
长期肌肉器官培养中的颤动和加速 AChR 降解。
DOI：
10.1002/mus.880141012
复制
发表时间：
1991
期刊：
影响因子：
3.4
通讯作者：
Salpeter,MM
中科院分区：
文献类型：
--
作者：
Wetzel,DM;Salpeter,MM
由于缺乏可用的体外制剂，对终板维持和重组的精确分子动力学评估受到限制。我们描述了小鼠膈肌的器官培养制剂，可以长期维持肌肉活力。在不同培养条件下评估了器官培养中自发性颤动、交界外乙酰胆碱受体水平增加、交界乙酰胆碱受体周转率加快以及器官培养中去神经小鼠膈肌精细结构的维持。在使用或不使用胎牛血清测试的几种标准组织培养基中，培养基 199 加胎牛血清最适合维持该肌肉超过 2 周。通过添加非葡萄糖能量底物（例如 D-b̃-羟基丁酸和 L-谷氨酰胺）可以部分消除血清成分。这种准备工作将允许对终板疾病的分子成分进行更可控的检查。
Evaluation of the precise molecular dynamics of endplate maintenance and reorganization has been limited by the lack of available in vitro preparations. We describe an organ culture preparation of mouse diaphragm muscle which permits long‐term maintenance of muscle viability. Spontaneous fibrillations, increased levels of extrajunctional acetylcholine receptors, accelerated rates of junctional acetylcholine receptor turnover and maintenance of fine structure of denervated mouse diaphragm muscle in organ culture was evaluated under different culture conditions. Of several standard tissue culture media tested with and without fetal calf serum, medium 199 plus fetal calf serum was best for maintaining this muscle for greater than 2 weeks. The serum component could be partially eliminated by addition of nonglucose energy substrates such as D‐b̃‐hydroxybutyric acid and L‐glutamine. This preparation will permit a more controlled examination of the molecular components of endplate diseases.