کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4341438 | 1295835 | 2006 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Delayed synapsing muscles are more severely affected in an experimental model of MuSK-induced myasthenia gravis
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
α-bungarotoxinSNMGα-BgTxMuSKAChRNMJPBSTPBSNeuromuscular junction - اتصال عصبی عضلانیAutoimmune disorders - اختلالات خود ایمنیanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancePhosphate buffered saline - فسفات بافر شورSeronegative myasthenia gravis - میاستنی گراوی صفراویMyasthenia gravis - میاستنی گراویسMuscle specific kinase - کیناز خاص عضلهMuscle-specific kinase - کیناز خاص ماهیچهacetylcholine receptor - گیرنده استیل کولینnicotinic acetylcholine receptor - گیرنده استیلکولین نیکوتینAgrin - یک نیشخند
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Delayed synapsing muscles are more severely affected in an experimental model of MuSK-induced myasthenia gravis Delayed synapsing muscles are more severely affected in an experimental model of MuSK-induced myasthenia gravis](/preview/png/4341438.png)
چکیده انگلیسی
Myasthenia gravis can be induced in mice by injecting the extracellular domain of rat muscle-specific kinase (MuSK), a transmembrane receptor tyrosine kinase involved in agrin signaling at the neuromuscular junction. About 5-10% of human myasthenia gravis patients have autoantibodies against MuSK. Here we have examined mouse neuromuscular junctions following MuSK immunization in two groups of muscles that can be distinguished on the basis of the timing of neuromuscular synaptogenesis and their response to perturbation of agrin signaling. We used confocal microscopy to characterize the distribution and expression of nicotinic acetylcoline receptors and of two presynaptic makers, neurofilament protein and synaptophysin. We observed disruption of neuromuscular junctions in all muscles examined in this model of myasthenia gravis. However delayed-synapsing muscles, including the diaphragm, sternomastoid and tibialis posterior, were significantly more severely affected than fast-synapsing muscles, including the intercostal, adductor longus and tibialis anterior. These results suggest a basis for the differential susceptibility of muscles in different classes of myasthenia gravis patients, including patients with autoantibodies against MuSK.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 143, Issue 3, 13 December 2006, Pages 655-659
Journal: Neuroscience - Volume 143, Issue 3, 13 December 2006, Pages 655-659
نویسندگان
K. Xu, S. Jha, W. Hoch, S.E. Dryer,