Survival of ganglion cells which form the retino-retinal projection during optic nerve regeneration in the frog

1993 ◽  
Vol 10 (4) ◽  
pp. 681-686 ◽  
Author(s):  
M. Tennant ◽  
S. R. Bruce ◽  
L. D. Beazley

AbstractDuring optic nerve regeneration in the frog, axons transiently grow along the opposite optic nerve forming a retino-retinal projection. In the present study, we crushed the left optic nerve in the frog Litoria (Hyla) moorei and later applied horseradish peroxidase (HRP) or diamidino yellow (DY) to the right optic nerve. In one series, retinae were examined 3 days after application of the tracer. The retino-retinal projection was found to be maximal at 5 weeks, fell significantly by 7 weeks, and returned to close-to-normal levels by 24 weeks. In a second series, we applied DY at 5 weeks as before but did not sacrifice the frogs until 7 weeks. Numbers of labeled ganglion cells were not significantly different from those frogs in the first series labeled and examined at 5 weeks. We conclude that ganglion cells giving rise to the retino-retinal projection had not died in appreciable numbers, presumably being sustained by collateral axons in the brain.

2021 ◽  
Vol 118 (9) ◽  
pp. e2017282118 ◽  
Author(s):  
Lili Xie ◽  
Yuqin Yin ◽  
Larry Benowitz

Ciliary neurotrophic factor (CNTF) is a leading therapeutic candidate for several ocular diseases and induces optic nerve regeneration in animal models. Paradoxically, however, although CNTF gene therapy promotes extensive regeneration, recombinant CNTF (rCNTF) has little effect. Because intraocular viral vectors induce inflammation, and because CNTF is an immune modulator, we investigated whether CNTF gene therapy acts indirectly through other immune mediators. The beneficial effects of CNTF gene therapy remained unchanged after deleting CNTF receptor alpha (CNTFRα) in retinal ganglion cells (RGCs), the projection neurons of the retina, but were diminished by depleting neutrophils or by genetically suppressing monocyte infiltration. CNTF gene therapy increased expression of C-C motif chemokine ligand 5 (CCL5) in immune cells and retinal glia, and recombinant CCL5 induced extensive axon regeneration. Conversely, CRISPR-mediated knockdown of the cognate receptor (CCR5) in RGCs or treating wild-type mice with a CCR5 antagonist repressed the effects of CNTF gene therapy. Thus, CCL5 is a previously unrecognized, potent activator of optic nerve regeneration and mediates many of the effects of CNTF gene therapy.


Cell Reports ◽  
2020 ◽  
Vol 31 (3) ◽  
pp. 107537 ◽  
Author(s):  
Xue-Wei Wang ◽  
Shu-Guang Yang ◽  
Chi Zhang ◽  
Ming-Wen Hu ◽  
Jiang Qian ◽  
...  

2007 ◽  
Vol 50 (5) ◽  
pp. 749-756 ◽  
Author(s):  
Yoshiki Koriyama ◽  
Keiko Homma ◽  
Kayo Sugitani ◽  
Yoshihiro Higuchi ◽  
Toru Matsukawa ◽  
...  

2017 ◽  
Vol 287 ◽  
pp. 365-373 ◽  
Author(s):  
Larry I. Benowitz ◽  
Zhigang He ◽  
Jeffrey L. Goldberg

1985 ◽  
Vol 344 (2) ◽  
pp. 267-280 ◽  
Author(s):  
Frank Scalia ◽  
Victoria Arango ◽  
Eric L. Singman

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