کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278159 | 1295796 | 2008 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tumor necrosis factor α enhances the sensitivity of rat trigeminal neurons to capsaicin
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کلمات کلیدی
NGFTNFRITumor necrosis factor receptor IITrigeminalTTXGAPDHTRPV1TNFα[Ca2+]i - [Ca2 +] iImmunoreactivity - ایمنی فعالtetrodotoxin - تترو دوتوکسین tumor necrosis factor α - تومور نکروز عامل αPain - دردCytokines - سیتوکین هاnerve growth factor - فاکتور رشد عصبHyperalgesia - پردردی یا هایپرآلژزیIntracellular calcium - کلسیم داخل سلولیtrigeminal ganglia - گانگلیس سه گانهglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Tumor necrosis factor α (TNFα), a pro-inflammatory cytokine, enhances the development of pain and hyperalgesia, although the molecular mechanisms are not well understood. This study evaluated the hypothesis that TNFα increases the sensitivity of rat trigeminal neurons to capsaicin via two different mechanisms triggered by either brief or sustained exposure to the cytokine. A brief (5 min) application of TNFα significantly sensitized capsaicin-evoked accumulation of intracellular calcium ([Ca2+]i) (226.4±37.7 nM vs. 167.5±31.3 nM) and increased capsaicin-evoked nocifensive behavior (78.3±9.7 vs. 30.9±3.6 s) as compared with vehicle pretreatment (P<0.01 for both). Sustained (30 min to 4 h) exposure of cultured neurons to TNFα evoked a twofold increase in mRNA transcript (P<0.05) and protein levels (P<0.01) of transient potential receptor vanilloid type 1 (TRPV1). This long-term up-regulation of TRPV1 expression by TNFα correlated with enhancement in capsaicin-induced calcitonin gene-related peptide release (P<0.05). Demonstration of colocalization of TNFα receptor subtypes I and II with TRPV1 in almost all (>90%) TRPV1 expressing neurons provides evidence consistent with a direct interaction on the same subpopulation of sensory neurons. In summary, our data demonstrate that TNFα directly enhances the sensitivity of rat trigeminal neurons to capsaicin via both rapid, non-genomic mechanisms as well as sustained genomic regulation in TRPV1 expression. Thus, increased sensitization and up-regulation of TRPV1 constitutes a potential mechanism by which TNFα mediates inflammatory hyperalgesia and pain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 155, Issue 2, 13 August 2008, Pages 503-509
Journal: Neuroscience - Volume 155, Issue 2, 13 August 2008, Pages 503-509
نویسندگان
A.A. Khan, A. Diogenes, N.A. Jeske, M.A. Henry, A. Akopian, K.M. Hargreaves,