4.5 Article

INTRAVITREOUS INTERLEUKIN-2 TREATMENT AND INFLAMMATION MODULATES GLIAL CELLS ACTIVATION AND UNCROSSED RETINOTECTAL DEVELOPMENT

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NEUROSCIENCE
卷 200, 期 -, 页码 223-236

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2011.10.034

关键词

IL-2; critical period; development; superior colliculus; plasticity; glial cells

资金

  1. FAPERJ (Fundacao Carlos Chagas Filho de Amparo a pesquisa do Estado do Rio de Janeiro)
  2. CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior)
  3. CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico)
  4. PRONEXIMCT
  5. PROPPi-UFF
  6. PIBIC/CNPq

向作者/读者索取更多资源

Interleukin-2 (IL-2) plays regulatory functions both in immune and nervous system. However, in the visual system, little is known about the cellular types which respond to IL-2 and its effects. Herein, we investigated the influence of IL-2 in the development of central visual pathways. Lister Hooded rats were submitted to multiple (at postnatal days [PND]7/10/13) or single (at PND10) intravitreous injections of phosphate-buffered saline (PBS) (vehicle), zymosan, or IL-2. IL-2 receptor alpha subunit was detected in the whole postnatal retina. Chronic treatment with either PBS or IL-2 increases retinal glial fibrillary acidic protein (GFAP) expression, induces intravitreous inflammation revealed by the presence of macrophages, and results in a slight rearrangement of retinotectal axons. Acute zymosan treatment disrupts retinotectal axons distribution, confirming the influence of inflammation on retinotectal pathway reordering. Furthermore, acute IL-2 treatment increases GFAP expression in the retina without inflammation and produces a robust sprouting of the intact uncrossed retinotectal pathway. No difference was observed in glial cells activity in superior colliculus. Taken together, these data suggest that inflammation and interleukin-2 modulate retinal ganglion cells development and the distribution of their axons within central targets. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

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