Interretinal transduction of injury signals after unilateral optic nerve crush

被引：30

作者：

Macharadze, Tamar ^{[1
]}

Goldschmidt, Juergen ^{[2
]}

Marunde, Monika ^{[1
]}

Wanger, Tim ^{[2
]}

Scheich, Henning ^{[2
]}

Zuschratter, Werner ^{[3
]}

Gundelfinger, Eckart D. ^{[4
]}

Kreutz, Michael R. ^{[1
]}

机构：

[1] Leibniz Inst Neurobiol, Project Grp Neuroplast, D-39118 Magdeburg, Germany

[2] Leibniz Inst Neurobiol, Dept Acoust Learning & Memory, D-39118 Magdeburg, Germany

[3] Leibniz Inst Neurobiol, Special Lab Confocal Laserscan Microscopy & Elect, D-39118 Magdeburg, Germany

[4] Leibniz Inst Neurobiol, Dept Neurochem & Mol Biol, D-39118 Magdeburg, Germany

来源：

NEUROREPORT | 2009年 / 20卷 / 03期

关键词：

inflammation; optic nerve crush; retinal ganglion cells; RETINAL GANGLION-CELLS; ALBINO-RATS; ADULT-RAT; REGENERATION; EXPRESSION; PROJECTION; SURVIVAL; PATHWAY;

D O I：

10.1097/WNR.0b013e32832027e6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In this study, we report that partial unilateral optic nerve crush in the rat affects the number of retinal ganglion cells of the contralateral eye still in continuity with the ipsilateral superior colliculus. The reduction in cell number of the uncrossed retinal projection was accompanied by a microglia response and could be prevented by the local intravitreal application of the anti-inflammatory agent dexamethasone. Interestingly, the level of neuronal activity after optic nerve crush as evidenced by thallium autometallography was enhanced in the termination area of the uncrossed projection, the rostro-medial superior colliculus, suggesting that a dying-back mechanism is not involved. We propose that injury signals from the damaged optic nerve and retina are transduced to the unaffected eye. NeuroReport 20:301-305 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

引用

页码：301 / 305

页数：5

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