کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9191999 | 1186609 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Intravitreal macrophage activation enables cat retinal ganglion cells to regenerate injured axons into the mature optic nerve
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Intravitreal macrophage activation enables cat retinal ganglion cells to regenerate injured axons into the mature optic nerve Intravitreal macrophage activation enables cat retinal ganglion cells to regenerate injured axons into the mature optic nerve](/preview/png/9191999.png)
چکیده انگلیسی
In mature mammals, retinal ganglion cells (RGCs) are generally unable to regenerate injured axons into the optic nerve. Here, we report that an intravitreal injection of either of two macrophage activators, oxidized galectin-1 or zymosan, strongly enhanced the regeneration of transected RGC axons beyond an optic nerve crush site in adult cats. Using WGA-HRP as an anterograde tracer, we found that injection of either macrophage activator caused many axons to grow into the distal optic nerve when evaluated 14 days later, with the strongest effects seen after injecting 100 ng of galectin-1. Elongation continued for at least another 2 weeks. Control eyes injected with saline contained very few labeled axons extending across the crush site. Elevation of intracellular cAMP levels using forskolin also enhanced regeneration beyond the crush site to some extent, but this treatment did not augment the effect of galectin-1 any further. These results indicate that RGCs of adult cats are capable of reverting to an active growth state and at least partially overcoming an inhibitory CNS environment as a result of intravitreal macrophage activation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 196, Issue 1, November 2005, Pages 153-163
Journal: Experimental Neurology - Volume 196, Issue 1, November 2005, Pages 153-163
نویسندگان
Takeshi Okada, Masahiro Ichikawa, Yoshihito Tokita, Hidenori Horie, Kiyoshi Saito, Jun Yoshida, Masami Watanabe,