BDNF Preserves the Dendritic Morphology of α and β Ganglion Cells in the Cat Retina after Optic Nerve Injury

2008 ◽  
Vol 49 (6) ◽  
pp. 2456 ◽  
Author(s):  
Arthur J. Weber ◽  
Christine D. Harman
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Ganglion Cells ◽  
Dendritic Morphology ◽  
Optic Nerve Injury ◽  
Cat Retina

scholarly journals Localized co-delivery of CNTF and FK506 using a thermosensitive hydrogel for retina ganglion cells protection after traumatic optic nerve injury

Drug Delivery ◽  
2020 ◽  
Vol 27 (1) ◽  
pp. 556-564
Author(s):  
Dongmei Wang ◽  
Mengmeng Luo ◽  
Baoshan Huang ◽  
Wa Gao ◽  
Yan Jiang ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Ganglion Cells ◽  
Optic Nerve Injury ◽  
Thermosensitive Hydrogel

Pyroglutamic Acid Promotes Survival of Retinal Ganglion Cells after Optic Nerve Injury

2009 ◽  
Vol 34 (7) ◽  
pp. 598-605 ◽  
Author(s):  
Shinichirou Oono ◽  
Takuji Kurimoto ◽  
Toru Nakazawa ◽  
Tomomitsu Miyoshi ◽  
Norio Okamoto ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Pyroglutamic Acid ◽  
Retinal Ganglion ◽  
Optic Nerve Injury

Early downregulation of IGF-I decides the fate of rat retinal ganglion cells after optic nerve injury

2007 ◽  
Vol 50 (5) ◽  
pp. 741-748 ◽  
Author(s):  
Keiko Homma ◽  
Yoshiki Koriyama ◽  
Kazuhiro Mawatari ◽  
Yoshihiro Higuchi ◽  
Jun Kosaka ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Optic Nerve Injury ◽  
Igf I

scholarly journals Protection of Pattern Electroretinogram and Retinal Ganglion Cells by Oncostatin M after Optic Nerve Injury

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e108524 ◽  
Author(s):  
Xin Xia ◽  
Rong Wen ◽  
Tsung-Han Chou ◽  
Yiwen Li ◽  
Zhengying Wang ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Pattern Electroretinogram ◽  
Oncostatin M ◽  
Retinal Ganglion ◽  
Optic Nerve Injury

Co-expression of c-Jun and ATF-2 characterizes the surviving retinal ganglion cells which maintain axonal connections after partial optic nerve injury

1999 ◽  
Vol 69 (2) ◽  
pp. 232-241 ◽  
Author(s):  
Michael R Kreutz ◽  
Annett Bien ◽  
Christian K Vorwerk ◽  
Tobias M Böckers ◽  
Constanze I Seidenbecher ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Optic Nerve Injury ◽  
Axonal Connections

scholarly journals Retinoic acid treatment recruits macrophages and increases axonal regeneration after optic nerve injury in the frog Rana pipiens

2021 ◽  
Author(s):  
Valeria De La Rosa-Reyes ◽  
Mildred V Duprey-Díaz ◽  
Jonathan M Blagburn ◽  
Rosa E Blanco
Keyword(s):  
Nervous System ◽  
Retinoic Acid ◽  
Optic Nerve ◽  
Nerve Injury ◽  
Phagocytic Activity ◽  
Axonal Regeneration ◽  
Ganglion Cells ◽  
System Development ◽  
Nervous System Development ◽  
Optic Nerve Injury

Retinoic acid (RA) plays major roles during nervous system development, and during regeneration of the adult nervous system. We have previously shown that components of the RA signaling pathway are upregulated after optic nerve injury, and that exogenous application of all-trans retinoic acid (ATRA) greatly increases the survival of axotomized retinal ganglion cells (RGCs). The objective of the present study is to investigate the effects of ATRA application on the macrophages in the optic nerve after injury, and to determine whether this affects axonal regeneration. The optic nerve was crushed and treated with PBS, ATRA and/or clodronate-loaded liposomes. Nerves were examined at one and two weeks after axotomy with light microscopy, immunocytochemistry and electron microscopy. ATRA application to the optic nerve caused transient increases in the number of macrophages and microglia one week after injury. The macrophages are consistently labeled with M2-type markers, and have considerable phagocytic activity. ATRA increased ultrastructural features of ongoing phagocytic activity in macrophages at one and two weeks. ATRA treatment also significantly increased the numbers of regenerating GAP-43-labeled axons. Clodronate liposome treatment depleted macrophage numbers by 80%, completely eliminated the ATRA-mediated increase in axonal regeneration, and clodronate treatment alone decreased axonal numbers by 30%. These results suggest that the success of axon regeneration is partially dependent on the presence of debris-phagocytosing macrophages, and that the increases in regeneration caused by ATRA are in part due to their increased numbers. Further studies will examine whether macrophage depletion affects RGC survival.

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