کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4341143 | 1295825 | 2008 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Evidence for a detrimental role of nitric oxide synthesized by endothelial nitric oxide synthase after peripheral nerve injury
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کلمات کلیدی
PBSMFRHCMVHMnETCO27-NIMean firing rateCMAPFluorogoldnNOSiNOSeGFPNOSeNOSL-NIO - 50-NIO7-nitroindazole - 7-نیتریدازولEnd-tidal CO2 - CO2 پایان یافتهd-NAME - D-NAMEl-NAME - L-NAMENω-nitro-l-arginine methyl ester - N-Nitro-L-Arginine Methyl EsterAdenovirus - آدنوویروسAminoguanidine - آمینوگوئیدینinducible isoform of nitric oxide synthase - ایزوفرم القا کننده سنتاز اکسید نیتریک استneuronal isoform of Nitric oxide synthase - ایزوفرم عصبی از سیتازاس اکسید نیتروژنphosphate buffer - بافر فسفاتAdenoviral vectors - بردارهای adenoviralHuman cytomegalovirus - سیتومگالوویروس انسانیHypoglossal nerve - عصب هیپوگلوزالیPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریhypoglossal motoneuron - موترونورون hypoglossalNitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازhypoglossal nucleus - هسته hypoglossalcompound muscle action potential - پتانسیل عمل عضله مرکبenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استperipheral neuropathy - پلینوریت
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Evidence for a detrimental role of nitric oxide synthesized by endothelial nitric oxide synthase after peripheral nerve injury Evidence for a detrimental role of nitric oxide synthesized by endothelial nitric oxide synthase after peripheral nerve injury](/preview/png/4341143.png)
چکیده انگلیسی
Physical injury to a nerve is the most common cause of acquired peripheral neuropathy. Identification of molecules involved in degenerative and regenerative processes is a key step toward development of therapeutic tools in order to accelerate motor, sensory and/or autonomic function recovery. We have studied the role of nitric oxide (NO) using as a model the severe crushing of a motor nerve in adult rats. This type of injury up-regulates the three isoforms of nitric oxide synthase (NOS) in the affected nerve. Chronic systemic inhibition of NOS accelerated the onset of functional muscle reinnervation evaluated by the recording of compound muscle action potential evoked by electrical stimulation of the injured nerve. Besides, it increased the number of back-labeled motoneurons by application, 2 days after injury, of a retrograde marker 10 mm distal to the crushing site. These effects were mimicked by chronic specific inhibition of the endothelial isoform of nitric oxide synthase (eNOS), but not by specific inhibitors of the neuronal or inducible isoform. Next, we intraneurally injected a replication-deficient adenoviral vector directing the expression of a dominant negative mutant of eNOS (Ad-TeNOS). A single injection of Ad-TeNOS on the day of crushing significantly accelerated functional recovery of neuromuscular junction and increased axonal regeneration. Moreover, Ad-TeNOS did not compromise motoneuron viability or stability of reestablished neuromuscular junctions. Taken together, these results suggest that NO of endothelial origin slows down muscle reinnervation by means of detrimental actions on axonal regeneration after peripheral nerve injury. These experiments identify eNOS as a potential therapeutic target for treatment of traumatic nerve injuries and highlight the potential of gene therapy in treating injuries of this type using viral vectors to suppress the activity of eNOS.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 157, Issue 1, 11 November 2008, Pages 40-51
Journal: Neuroscience - Volume 157, Issue 1, 11 November 2008, Pages 40-51
نویسندگان
C.R. Sunico, F. Portillo, D. González-Forero, S. Kasparov, B. Moreno-López,