scholarly journals Application of Rho Antagonist to Neuronal Cell Bodies Promotes Neurite Growth in Compartmented Cultures and Regeneration of Retinal Ganglion Cell Axons in the Optic Nerve of Adult Rats

2005 ◽  
Vol 25 (5) ◽  
pp. 1113-1121 ◽  
Author(s):  
J. Bertrand
1995 ◽  
Vol 73 (9-10) ◽  
pp. 599-604 ◽  
Author(s):  
Michael Minzenberg ◽  
Michelle Berkelaar ◽  
Garth Bray ◽  
Lisa Mckerracher

After injury in the central nervous system of adult mammals, many of the axons that remain attached to their intact cell bodies degenerate and decrease in calibre. To understand this process better, we have investigated the relationship between axonal loss, cell loss, and the time course of changes in axonal calibre. Optic nerves (ONs) were crushed and the numbers and sizes of axons remaining close to the cell bodies (2 mm from the eye) and near the site of the lesion (6 mm from the eye) were determined for nerves examined between 1 week and 3 months after injury. Comparison with the retinal ganglion cell (RGC) counts from the same animals revealed that axonal loss was concomitant with cell body loss for at least the first 2 weeks after injury. However, there was no significant change in the calibre of the surviving neurons until 1 month after injury. Thereafter, the axonal calibre was decreased equally along the ON. No progressive somatofugal atrophy was observed. These decreases in axonal calibre occur much later than the immediate drop in neurofilament (NF) expression that also follows injury. The late effect of injury on axonal calibre suggests that NF expression is not the sole determinant of axon size of the RGC fibers in the ON. Other factors are likely additional contributing factors, such as the decreased rate of axonal transport that would help maintain the axonal neurofilament content.Key words: axonal calibre, axotomy, neuronal cell death, neurofilaments, retinal ganglion cell, optic nerve.


1993 ◽  
Vol 24 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Maria-Paz Villegas-Pérez ◽  
Manuel Vidal-Sanz ◽  
Michael Rasminsky ◽  
Garth M. Bray ◽  
Albert J. Aguayo

2017 ◽  
Vol 426 (2) ◽  
pp. 360-373 ◽  
Author(s):  
G.B. Whitworth ◽  
B.C. Misaghi ◽  
D.M. Rosenthal ◽  
E.A. Mills ◽  
D.J. Heinen ◽  
...  

2017 ◽  
Vol 162 ◽  
pp. 97-103 ◽  
Author(s):  
Zhen Puyang ◽  
Hai-Qing Gong ◽  
Shi-Gang He ◽  
John B. Troy ◽  
Xiaorong Liu ◽  
...  

2018 ◽  
Vol 59 (3) ◽  
pp. 1562 ◽  
Author(s):  
Min H. Kang ◽  
Mengchen Suo ◽  
Chandrakumar Balaratnasingam ◽  
Paula K. Yu ◽  
William H. Morgan ◽  
...  

2015 ◽  
Vol 56 (10) ◽  
pp. 6095 ◽  
Author(s):  
Francisco M. Nadal-Nicolás ◽  
Paloma Sobrado-Calvo ◽  
Manuel Jiménez-López ◽  
Manuel Vidal-Sanz ◽  
Marta Agudo-Barriuso

Author(s):  
Tian Wang ◽  
Yiming Li ◽  
Miao Guo ◽  
Xue Dong ◽  
Mengyu Liao ◽  
...  

Traumatic optic neuropathy (TON) refers to optic nerve damage caused by trauma, leading to partial or complete loss of vision. The primary treatment options, such as hormonal therapy and surgery, have limited efficacy. Pituitary adenylate cyclase-activating polypeptide 38 (PACAP38), a functional endogenous neuroprotective peptide, has emerged as a promising therapeutic agent. In this study, we used rat retinal ganglion cell (RGC) exosomes as nanosized vesicles for the delivery of PACAP38 loaded via the exosomal anchor peptide CP05 (EXOPACAP38). EXOPACAP38 showed greater uptake efficiency in vitro and in vivo than PACAP38. The results showed that EXOPACAP38 significantly enhanced the RGC survival rate and retinal nerve fiber layer thickness in a rat TON model. Moreover, EXOPACAP38 significantly promoted axon regeneration and optic nerve function after injury. These findings indicate that EXOPACAP38 can be used as a treatment option and may have therapeutic implications for patients with TON.


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