کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5813407 | 1556610 | 2016 | 42 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Stress induces analgesia via orexin 1 receptor-initiated endocannabinoid/CB1 signaling in the mouse periaqueductal gray
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کلمات کلیدی
2-arachidonoylglycerol1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-1-piperidinyl-1H-pyrazole-3-carboxamideOX1 receptorNaloxone (PubChem CID: 5464092)SIASB 334867vlPAGPLCMPE2-AGAM 251 - 251 مAUC - AUCDAGL - NEC روزانهWIN 55,212-2 - WIN 55،212-2Orexin - اورکسینstress-induced analgesia - بی اشتهایی ناشی از استرسperiaqueductal gray - خاکستری پرآبیVentrolateral periaqueductal gray - خاکستری پرآلکتونی VentrolateralPain - دردdiacylglycerol - دیسیل گلیسیرینDAG - روزphospholipase C - فسفولیپاز Cdiacylglycerol lipase - لیپاز دی سیل گلیسرولarea under the curve - منطقه تحت منحنیCannabinoid - کانابینوئیدCB1 receptor - گیرنده CB1Orexin 1 receptor - گیرنده اورکسین 1Orexin 2 receptor - گیرنده اورکسین 2Cannabinoid 1 receptor - گیرنده کانابینوئید 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
The orexin system consists of orexin A/hypocretin 1 and orexin B/hypocretin 2, and OX1 and OX2 receptors. Our previous electrophysiological study showed that orexin A in the rat ventrolateral periaqueductal gray (vlPAG) induced antinociception via an OX1 receptor-initiated and endocannabinoid-mediated disinhibition mechanism. Here, we further characterized antinociceptive effects of orexins in the mouse vlPAG and investigated whether this mechanism in the vlPAG can contribute to stress-induced analgesia (SIA) in mice. Intra-vlPAG (i.pag.) microinjection of orexin A in the mouse vlPAG increased the hot-plate latency. This effect was mimicked by i.pag. injection of WIN 55,212-2, a CB1 agonist, and antagonized by i.pag. injection of the antagonist of OX1 (SB 334867) or CB1 (AM 251), but not OX2 (TCS-OX2-29) or opioid (naloxone), receptors. [Ala11, D-Leu15]-orexin B (i.pag.), an OX2 selective agonist, also induced antinociception in a manner blocked by i.pag. injection of TCS-OX2-29, but not SB 334867 or AM 251. Mice receiving restraint stress for 30Â min showed significantly longer hot-plate latency, more c-Fos-expressing orexin neurons in the lateral hypothalamus and higher orexin levels in the vlPAG than unrestrained mice. Restraint SIA in mice was prevented by i.pag. or intraperitoneal injection of SB 334867 or AM 251, but not TCS-OX2-29 or naloxone. These results suggest that during stress, hypothalamic orexin neurons are activated, releasing orexins into the vlPAG to induce analgesia, possibly via the OX1 receptor-initiated, endocannabinoid-mediated disinhibition mechanism previously reported. Although activating either OX1 or OX2 receptors in the vlPAG can lead to antinociception, only OX1 receptor-initiated antinociception is endocannabinoid-dependent.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropharmacology - Volume 105, June 2016, Pages 577-586
Journal: Neuropharmacology - Volume 105, June 2016, Pages 577-586
نویسندگان
Hsin-Jung Lee, Lu-Yang Chang, Yu-Cheng Ho, Shu-Fang Teng, Ling-Ling Hwang, Ken Mackie, Lih-Chu Chiou,