کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4340740 | 1295808 | 2008 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Spinal nerve ligation-induced activation of nuclear factor kappaB is facilitated by prostaglandins in the affected spinal cord and is a critical step in the development of mechanical allodynia
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کلمات کلیدی
PGE2PDTCSGCPWTSNLiNOSCOX-1COX-2COXDRGDMSO - DMSONFκB - NFKBpaw withdrawal threshold - آستانه برداشتن پاAllodynia - آلودینیا cyclooxygenase - آنزیم سیکلواکسیژنازi.t. - آی تی.intrathecal - اینتراکتالanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceDimethyl sulfoxide - دیمتیل سولفواکسیدinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییSoluble guanylate cyclase - سیکلاس گوانیلات حل کنندهcyclooxygenase-1 - سیکلوکوکسیژناز 1Cyclooxygenase-2 - سیکلوکوکسیژناز2nuclear factor kappaB - فاکتور هسته ای kappaBProstaglandin E2 - پروستاگلاندین E2prostaglandin - پروستاگلاندینهاspinal nerve ligation - پیوند عصب ستون فقراتdorsal root ganglia - گانگلیس ریشه پشتی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
This study investigated the effect of 5th and 6th lumbar nerve (L5/L6) spinal nerve ligation (SNL) on activated nuclear factor kappaB (NFkBa) in nuclear extracts from the lumbar dorsal horn of the rat, and its relationship to prostaglandin (PG)-dependent spinal hyperexcitability and allodynia 3 days later. Male Sprague-Dawley rats, fitted with intrathecal (i.t.) catheters, underwent SNL- or sham-surgery. Paw withdrawal threshold (PWT), electromyographic analysis of the biceps femoris flexor reflex, and immunoblotting of the spinal cord were used. Both allodynia (PWT â¤4 g) and exaggerated A- and C-fiber-mediated reflex responses (AFRR and CFRR), featuring decreased activation thresholds and evoked hyperexcitability, were evident only in nerve-ligated animals. This was preceded by an increase in NFkBa in the ipsilateral lumbar dorsal horn at 12 h which was still present 3 days after SNL. The amount of NFkBa in the ventral horns was unchanged compared with sham-controls. Blocking the activation of spinal NFκB, either directly with ammonium pyrrolidedithiocarbamate (PDTC; 100 μg i.t.) or indirectly with S(+)-ibuprofen (100 μg i.t.) administered immediately after SNL, prevented the SNL-induced expression of spinal cyclooxygenase-2 and the development of spinal hyperexcitability and allodynia 3 days later. R(â)-Ibuprofen and vehicle had no effect. These results demonstrate that NFκB is not only activated by SNL, but that spinal PG generated in the affected spinal cord from the onset of nerve injury facilitates this process. NFκB is a critical antecedent in the development of spinal PG-dependent hyperexcitability and allodynia in the SNL model.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 155, Issue 3, 26 August 2008, Pages 902-913
Journal: Neuroscience - Volume 155, Issue 3, 26 August 2008, Pages 902-913
نویسندگان
D.D. O'Rielly, C.W. Loomis,