کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4341017 | 1614907 | 2007 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Essential role of mu opioid receptor in the regulation of delta opioid receptor-mediated antihyperalgesia
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کلمات کلیدی
DRGpro-enkephalinDeltorphin IIβ-ENDintrathecallyd-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH2antihyperalgesiaCTOPpDynMORCFAdorsal root ganglion - گانگلیون ریشه پشتیcomplete Freund’s adjuvant - adjuvant دوست کاملDAMGO - DREAMβ-endorphin - β-آندورفینi.t. - آی تی.inflammation - التهاب( توروم) DOR - دردKOR - وقتیPENK - پینکkappa opioid receptor - گیرنده اپوئیدی کاپاپMu opioid receptor - گیرنده اپیدمی مdelta opioid receptor - گیرنده دلتا اپیوئید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Analgesic effects of delta opioid receptor (DOR) -selective agonists are enhanced during persistent inflammation and arthritis. Although the underlying mechanisms are still unknown, membrane density of DOR was shown to be increased 72 h after induction of inflammation, an effect abolished in mu opioid receptor (MOR) -knockout (KO) mice [Morinville A, Cahill CM, Kieffer B, Collier B, Beaudet A (2004b) Mu-opioid receptor knockout prevents changes in delta-opioid receptor trafficking induced by chronic inflammatory pain. Pain 109:266-273]. In this study, we demonstrated a crucial role of MOR in DOR-mediated antihyperalgesia. Intrathecal administration of the DOR selective agonist deltorphin II failed to induce antihyperalgesic effects in MOR-KO mice, whereas it dose-dependently reversed thermal hyperalgesia in wild-type mice. The antihyperalgesic effects of deltorphin II were blocked by naltrindole but not d-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) suggesting that this agonist was mainly acting through DOR. SNC80-induced antihyperalgesic effects in MOR-KO mice were also attenuated as compared with littermate controls. In contrast, kappa opioid receptor knockout did not affect deltorphin II-induced antihyperalgesia. As evaluated using mice lacking endogenous opioid peptides, the regulation of DOR's effects was also independent of β-endorphin, enkephalins, or dynorphin opioids known to be released during persistent inflammation. We therefore conclude that DOR-mediated antihyperalgesia is dependent on MOR expression but that activation of MOR by endogenous opioids is probably not required.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 150, Issue 4, 19 December 2007, Pages 807-817
Journal: Neuroscience - Volume 150, Issue 4, 19 December 2007, Pages 807-817
نویسندگان
L. Gendron, J.E. Pintar, C. Chavkin,