کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5737400 | 1614711 | 2017 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibition of Nkcc1 promotes axonal growth and motor recovery in ischemic rats
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
oligodendrocyte-myelin glycoproteinLSDOMgpPVDF4,6-diamino-2-phenyl indoleNKCC1BDAMAGDAPIET-1MCAOKCC2CSt - CSTgamma-aminobutyric acid - اسید گاما آمینو بوتیریکendothelin-1 - اندوتلین-1middle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیFunctional recovery - بهبود عملکردBumetanide - بومتانییدbiotinylated dextran amine - بیوترنیته دیستران آمینleast significant difference - حداقل تفاوت قابل توجهیcorticospinal tract - دستگاه گوارشAxonal growth - رشد AxonalBBB - سد خونی مغزیStroke - سکته مغزیblood–brain-barrier - مانع خون مغزیPolyvinylidene fluoride - پلی وینیلیدین فلورایدRho-associated kinase - کیناز وابسته به RhoGABA - گاباMyelin-associated glycoprotein - گلیکوپروتئین مرتبط با میلینRock - یا راک
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Bumetanide is a selective inhibitor of the Na+-K+-Clâ-co-transporter 1(NKCC1). We studied whether bumetanide could affect axonal growth and behavioral outcome in stroke rats. Adult male Wistar rats were randomly assigned to four groups: sham-operated rats treated with vehicle or bumetanide, and ischemic rats treated with vehicle or bumetanide. Endothelin-1 was used to induce focal cerebral ischemia. Bumetanide administration (i.c.v.) started on postoperative day 7 and continued for 3 weeks. Biotinylated dextran amine (BDA) was injected into the right imotor cortex on postoperative day 14 to trace corticospinal tract (CST) fibers sprouting into the denervated cervical spinal cord. Nogo-A, NKCC1, KCC2 and BDNF in the perilesional cortex and BDA, PSD-95 and vGlut1 in the denervated spinal cord were measured by immunohistochemistry and/or Western blot. Behavioral outcome of rats was assessed by the beam walking and cylinder tests. The total length of CST fibers sprouting into the denervated cervical spinal cord significantly increased after stroke and bumetanide further increased this sprouting. Bumetanide treatment also decreased the expressions of NKCC1 and Nogo-A, increased the expressions of KCC2 and BDNF in the perilesional cortex and enhanced the synaptic plasticity in the denervated cervical spinal cord after cerebral ischemia. The behavioral performance of ischemic rats was significantly improved by bumetanide. In conclusion, bumetanide promoted post-stroke axonal sprouting together accompanied by an improved behavioral outcome possibly through restoring and maintaining neuronal chloride homeostasis and creating a recovery-promoting microenvironment by overcoming the axonal growth inhibition encountered after cerebral ischemia in rats.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 365, 4 December 2017, Pages 83-93
Journal: Neuroscience - Volume 365, 4 December 2017, Pages 83-93
نویسندگان
X.P. Mu, H.B. Wang, X. Cheng, L. Yang, X.Y. Sun, H.L. Qu, S.S. Zhao, Z.K. Zhou, T.T. Liu, T. Xiao, B. Song, J. Jolkkonen, C.S. Zhao,