کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6016825 | 1580152 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A new model of nerve injury in the rat reveals a role of Regulator of G protein Signaling 4 in tactile hypersensitivity
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کلمات کلیدی
DRGRGS4SNIIBA1RGSPWTSSIGFAPMPEdorsal root ganglion - گانگلیون ریشه پشتیpaw withdrawal threshold - آستانه برداشتن پاSpared nerve injury - آسیب عصب آسیب دیدهAllodynia - آلودینیا Neuropathic pain - درد نوروپاتیکChronification - زمان کوتاه شدنAnimal model - مدل حیوانیionized calcium-binding adapter molecule 1 - ملکول آداپتور اتصال دهنده کلسیم یونیزه 1Glial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالCB1 receptor - گیرنده CB1cannabinoid type-1 receptor - گیرنده نوع 1 کانابینوئیدGlia - یاختههای گلیال
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: A new model of nerve injury in the rat reveals a role of Regulator of G protein Signaling 4 in tactile hypersensitivity A new model of nerve injury in the rat reveals a role of Regulator of G protein Signaling 4 in tactile hypersensitivity](/preview/png/6016825.png)
چکیده انگلیسی
Tactile hypersensitivity is one of the most debilitating symptoms of neuropathic pain syndromes. Clinical studies have suggested that its presence at early postoperative stages may predict chronic (neuropathic) pain after surgery. Currently available animal models are typically associated with consistent tactile hypersensitivity and are therefore limited to distinguish between mechanisms that underlie tactile hypersensitivity as opposed to mechanisms that protect against it. In this study we have modified the rat model of spared nerve injury, restricting the surgical lesion to a single peripheral branch of the sciatic nerve. This modification reduced the prevalence of tactile hypersensitivity from nearly 100% to approximately 50%. With this model, we here also demonstrated that the Regulator of G protein Signaling 4 (RGS4) was specifically up-regulated in the lumbar dorsal root ganglia and dorsal horn of rats developing tactile hypersensitivity. Intrathecal delivery of the RGS4 inhibitor CCG63802 was found to reverse tactile hypersensitivity for a 1Â h period. Moreover, tactile hypersensitivity after modified spared nerve injury was most frequently persistent for at least four weeks and associated with higher reactivity of glial cells in the lumbar dorsal horn. Based on these data we suggest that this new animal model of nerve injury represents an asset in understanding divergent neuropathic pain outcomes, so far unravelling a role of RGS4 in tactile hypersensitivity. Whether this model also holds promise in the study of the transition from acute to chronic pain will have to be seen in future investigations.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 286, December 2016, Pages 1-11
Journal: Experimental Neurology - Volume 286, December 2016, Pages 1-11
نویسندگان
Giuliano Taccola, Pierre J Doyen, Jonathan Damblon, Nejada Dingu, Beatrice Ballarin, Arnaud Steyaert, Anne des Rieux, Patrice Forget, Emmanuel Hermans, Barbara Bosier, Ronald Deumens,