کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5813778 | 1556616 | 2015 | 49 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Involvement of p38 MAPK activation mediated through AT1 receptors on spinal astrocytes and neurons in angiotensin II- and III-induced nociceptive behavior in mice
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کلمات کلیدی
c-Jun N-terminus kinaseAT1AT2NDSNeuNECLID50LAAi.p.ERKHRPACENGSGFAPJnkDMSO - DMSOIba-1 - IBA-1MAPK - MAPKp38 MAPK - P38 MAPKAstrocyte - آستروسیتangiotensin - آنژیوتانسینAngiotensin III - آنژیوتانسین IIIAngiotensin II - آنژیوتانسین دوi.t. - آی تی.immunoreactive - ایمنی فعالAng - اینintrathecal - اینتراکتالenhanced chemiluminescence - بهبود شیمیایی لومنIntrathecal administration - تزریق داخل رحمیintraperitoneal - داخل صفاقیDimethyl sulfoxide - دیمتیل سولفواکسیدNociceptive behavior - رفتار ناسازگارانهnormal goat serum - سرم طبیعی بزnormal donkey serum - سرم عسل طبیعیMice - موشionized calcium binding adaptor molecule 1 - مولکول آداپتور اتصال دهنده کلسیم یونیزه 1Neuron - نورونneuronal nuclei - هسته های نورونیHorseradish peroxidase - پراکسیداز هوررادیشGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیAT1 receptors - گیرنده AT1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
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چکیده انگلیسی
We have previously demonstrated the possibility that angiotensin (Ang) II and its N-terminal metabolite Ang (1-7) act as neurotransmitters and/or neuromodulators in the spinal transmission of nociceptive information. Ang III, which is a C-terminal metabolite of Ang II, can also act on AT1 receptors, but its role in spinal nociceptive transmission remains unclear. Therefore, we examined the role of Ang III on the spinal nociceptive system in comparison with that of Ang II. Intrathecal (i.t.) administration of Ang III into mice produced a nociceptive behavior, which was dose-dependently inhibited by the co-administration of the AT1 receptor antagonist losartan and the p38 MAPK inhibitor SB203580, but not by the AT2 receptor antagonist PD123319, MEK1/2 inhibitor U0126 and JNK inhibitor SP600125. In addition, Ang III increased the phosphorylation of p38 MAPK in the dorsal lumbar spinal cord, which was inhibited by losartan. These effects were similar to those of observed with Ang II. The nociceptive behavior produced by Ang II or III was also attenuated by the administration of the astrocytic inhibitor l-α-aminoadipic acid, but not by the microglial inhibitor minocycline. Double immunohistochemical staining showed that spinal AT1 receptors were expressed on neurons and astrocytes, and that i.t. administration of either Ang II or III phosphorylated p38 MAPK in both spinal astrocytes and neurons. These results indicate that Ang III produces nociceptive behavior similar to Ang II, and suggest that the phosphorylation of p38 MAPK mediated through AT1 receptors on spinal astrocytes and neurons contributes to Ang II- and III-induced nociceptive behavior.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropharmacology - Volume 99, December 2015, Pages 221-231
Journal: Neuropharmacology - Volume 99, December 2015, Pages 221-231
نویسندگان
Wataru Nemoto, Yoshiki Ogata, Osamu Nakagawasai, Fukie Yaoita, Takeshi Tadano, Koichi Tan-No,