کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5737543 | 1614736 | 2017 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
ERK potentiates p38 in central sensitization induced by traumatic occlusion
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کلمات کلیدی
CFAUACERKPPTcomplete Freund’s adjuvant - adjuvant دوست کاملMAPK - MAPKAdenosine Triphosphate - آدنوزین تری فسفاتATP - آدنوزین تری فسفات یا ATPOcclusal trauma - آسیب اکلوزالیpressure pain threshold - فشار آستانه دردtemporomandibular joint - مفصل گیجگاهیMicroglia - میکروگلیاهاNeuron - نورونHyperalgesia - پردردی یا هایپرآلژزیp38 mitogen-activated protein kinase (MAPK) - پروتئین کیناز فعال میتوژنز P38 (MAPK)p38 mitogen-activated protein kinase - پروتئین کیناز متیوژن فعال p38Polyethylene - پلی اتیلنextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیExtracellular signal-regulated kinase (ERK) - کیناز تنظیم شده سیگنال خارج سلولی (ERK)
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
This study was to investigate the role of p38 activation via ERK1/2 phosphorylation in neurons and microglia of the spinal trigeminal subnucleus caudalis (Vc) in the promotion of orofacial hyperalgesia induced by unilateral anterior crossbite (UAC) traumatic occlusion in adult rats. U0126, a p-ERK1/2 inhibitor, was injected intracisternally before UAC implant. The effects of the U0126 injection were compared to those following the injection of SB203580, a p-p38 inhibitor. Mechanical hyperalgesia was evaluated via pressure pain threshold measurements. Brain stem tissues were processed for a Western blot analysis to evaluate the activation of ERK1/2 and p38. Double immunofluorescence was also performed to observe the expression of p-ERK1/2 and p-p38 in neurons (labeled by NeuN) and microglia (labeled by OX42). The data showed that UAC caused orofacial hyperalgia ipsilaterally on d1 to d7, peaking on d3 (PÂ <Â 0.05). An upregulation of p-ERK1/2 was observed in the ipsilateral Vc on d1 to d3, peaking on d1. An upregulation of p-p38 was also observed on d1 to d7, peaking on d3 (PÂ <Â 0.05). p-ERK1/2 primarily co-localized with NeuN and, to a lesser extent, with OX42, while p-p38 co-localized with both NeuN and OX42. Pretreatment with U0126 prevented the upregulation of both p-ERK1/2 and p-p38. Similarly to an intracisternal injection of SB203580, U0126 pretreatment attenuated the UAC-induced orofacial hyperalgesia. These data indicate that UAC caused orofacial hyperalgesia by inducing central sensitization via the activation of ERK1/2 and p38 in both neurons and microglia in the Vc, potentially impacting the effects of p-ERK1/2 during p38 activation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 340, 6 January 2017, Pages 445-454
Journal: Neuroscience - Volume 340, 6 January 2017, Pages 445-454
نویسندگان
Lei Jing, Xiao-Dong Liu, Hong-Xu Yang, Mian Zhang, Ying Wang, Li Duan, Jing Zhang, Lei Lu, Ting Yang, Dong-Mei Wang, Liang-Wei Chen, Mei-Qing Wang,