کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6277881 | 1295777 | 2009 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Functional recovery of callosal axons following demyelination: a critical window
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کلمات کلیدی
Corpus callosumPBSMOGwksPFAAxon damageOLPGST-piβ-APPdemyelination - demyelinimasRemyelination - RemyelinimasOligodendrocyte - الیگودندروسیتNeurodegeneration - تولید نوروژنیکPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریMultiple sclerosis - مولتیپل اسکلروزیس(ام اس)weeks - هفته هاparaformaldehyde - پارافرمالدهیدCompound Action Potential - پتانسیل اقدام مشترکaction potential - پتانسیل عمل oligodendrocyte progenitor - پیشگام اولیگودندروسیتCaP - کلاه لبه دارmyelin oligodendrocyte glycoprotein - گلیکوپروتئین الیگودندروسیت میلین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Functional recovery of callosal axons following demyelination: a critical window Functional recovery of callosal axons following demyelination: a critical window](/preview/png/6277881.png)
چکیده انگلیسی
Axonal dysfunction as a result of persistent demyelination has been increasingly appreciated as a cause of functional deficit in demyelinating diseases such as multiple sclerosis. Therefore, it is crucial to understand the ultimate causes of ongoing axonal dysfunction and find effective measures to prevent axon loss. Our findings related to functional deficit and functional recovery of axons from a demyelinating insult are important preliminary steps towards understanding this issue. Cuprizone diet for 3-6 wks triggered extensive corpus callosum (CC) demyelination, reduced axon conduction, and resulted in loss of axon structural integrity including nodes of Ranvier. Replacing cuprizone diet with normal diet led to regeneration of myelin, but did not fully reverse the conduction and structural deficits. A shorter 1.5 wk cuprizone diet also caused demyelination of the CC, with minimal loss of axon structure and nodal organization. Switching to normal diet led to remyelination and restored callosal axon conduction to normal levels. Our findings suggest the existence of a critical window of time for remyelination, beyond which demyelinated axons become damaged beyond the point of repair and permanent functional loss follows. Moreover, initiating remyelination early within the critical period, before prolonged demyelination-induced axon damage ensues, will improve functional axon recovery and inhibit disease progression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 164, Issue 4, 29 December 2009, Pages 1407-1421
Journal: Neuroscience - Volume 164, Issue 4, 29 December 2009, Pages 1407-1421
نویسندگان
D.K. Crawford, M. Mangiardi, X. Xia, H.E. López-Valdés, S.K. Tiwari-Woodruff,