Wieczorek D F
Muscle Nerve. 1984 Mar-Apr;7(3):179-93. doi: 10.1002/mus.880070302.
Muscular dysgenesis (mdg), a disease expressed in embryonic mice, severely affects the formation and differentiation of skeletal musculature. The focus of this investigation was an analysis of dysgenic nervous tissue with special attention centered on interactions between muscle and nerve cells in vitro. Results indicate that mdg/mdg spinal cord cells can form functional neuromuscular junctions in nerve-muscle cocultures and induce contractions in dysgenic muscle. However, dysgenic spinal cord cells induce fewer myotubes to contract and result in a delayed induction of dysgenic myotube contractile activity. Furthermore, mdg/mdg nervous tissue, or its conditioned medium, is associated with a higher incidence of morphologically abnormal myotube contractures. The results from this investigation demonstrate that there are functional abnormalities in both dysgenic muscle and nervous tissues which are stable and expressed for up to 3 weeks in vitro.
肌肉发育不全(mdg)是一种在胚胎小鼠中表现出的疾病,严重影响骨骼肌肉组织的形成和分化。本研究的重点是分析发育不全的神经组织,特别关注体外肌肉与神经细胞之间的相互作用。结果表明,mdg/mdg脊髓细胞可在神经-肌肉共培养物中形成功能性神经肌肉接头,并诱导发育不全的肌肉收缩。然而,发育不全的脊髓细胞诱导收缩的肌管较少,并导致发育不全的肌管收缩活性诱导延迟。此外,mdg/mdg神经组织或其条件培养基与形态异常的肌管挛缩发生率较高有关。本研究结果表明,发育不全的肌肉和神经组织均存在功能异常,这些异常在体外是稳定的,并且可持续表达长达3周。