کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6274771 | 1614828 | 2013 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Deficient functional recovery after facial nerve crush in rats is associated with restricted rearrangements of synaptic terminals in the facial nucleus
ترجمه فارسی عنوان
بهبود عملکرد عملکردی ناخوشایند پس از شکستن عصب صورت در موشها با تغییرات محدودی پایانه های سیناپسی در هسته صورت همراه است
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کلمات کلیدی
Tenascin-RTNRVGLUTIBA1LLSstandard deviation - انحراف معیارPeripheral nerve regeneration - بازسازی عصب محیطیanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceVolume - جلدvesicular glutamate transporter - حمل و نقل گلوتامات vesicularvesicular glutamate transporter 2 - حمل کننده گلوتامات vesicular 2CNS - دستگاه عصبی مرکزیcentral nervous system - سیستم عصبی مرکزیCholinergic synapses - سیناپسهای کولینرژیکNumber - عددionized calcium binding adaptor molecule 1 - مولکول آداپتور اتصال دهنده کلسیم یونیزه 1Microglia - میکروگلیاهاWhisking - ویسکیSynaptic plasticity - پلاستیسیته سیناپسیChAT - چتnumerical density - چگالی عددیcholine acetyltransferase - کولین استیل ترانسفراز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Crush injuries of peripheral nerves typically lead to axonotmesis, axonal damage without disruption of connective tissue sheaths. Generally, human patients and experimental animals recover well after axonotmesis and the favorable outcome has been attributed to precise axonal reinnervation of the original peripheral targets. Here we assessed functionally and morphologically the long-term consequences of facial nerve axonotmesis in rats. Expectedly, we found that 5Â months after crush or cryogenic nerve lesion, the numbers of motoneurons with regenerated axons and their projection pattern into the main branches of the facial nerve were similar to those in control animals suggesting precise target reinnervation. Unexpectedly, however, we found that functional recovery, estimated by vibrissal motion analysis, was incomplete at 2Â months after injury and did not improve thereafter. The maximum amplitude of whisking remained substantially, by more than 30% lower than control values even 5Â months after axonotmesis. Morphological analyses showed that the facial motoneurons ipsilateral to injury were innervated by lower numbers of glutamatergic terminals (â15%) and cholinergic perisomatic boutons (â26%) compared with the contralateral non-injured motoneurons. The structural deficits were correlated with functional performance of individual animals and associated with microgliosis in the facial nucleus but not with polyinnervation of muscle fibers. These results support the idea that restricted CNS plasticity and insufficient afferent inputs to motoneurons may substantially contribute to functional deficits after facial nerve injuries, possibly including pathologic conditions in humans like axonotmesis in idiopathic facial nerve (Bell's) palsy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 248, 17 September 2013, Pages 307-318
Journal: Neuroscience - Volume 248, 17 September 2013, Pages 307-318
نویسندگان
G. Hundeshagen, K. Szameit, H. Thieme, M. Finkensieper, D.N. Angelov, O. Guntinas-Lichius, A. Irintchev,