scholarly journals Axon regeneration across the site of injury in the optic nerve of the newt Triturus pyrrhogaster

1977 ◽  
Vol 179 (4) ◽  
Author(s):  
L.J. Stensaas ◽  
E.R. Feringa
Keyword(s):  
Optic Nerve ◽  
Axon Regeneration ◽  
Triturus Pyrrhogaster

Neuronal, but not glial Contactin 2, negatively regulates axon regeneration in the injured adult optic nerve

2021 ◽  
Author(s):  
Maria Savvaki ◽  
George Kafetzis ◽  
Stefanos‐Ioannis Kaplanis ◽  
Niki Ktena ◽  
Kostas Theodorakis ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Axon Regeneration

scholarly journals Exosome-Mediated Delivery of the Neuroprotective Peptide PACAP38 Promotes Retinal Ganglion Cell Survival and Axon Regeneration in Rats With Traumatic Optic Neuropathy

2021 ◽  
Vol 9 ◽  
Author(s):  
Tian Wang ◽  
Yiming Li ◽  
Miao Guo ◽  
Xue Dong ◽  
Mengyu Liao ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Optic Neuropathy ◽  
Axon Regeneration ◽  
Retinal Ganglion ◽  
Traumatic Optic Neuropathy ◽  
Fiber Layer

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.

Inhibition of miR-21 ameliorates excessive astrocyte activation and promotes axon regeneration following optic nerve crush

2018 ◽  
Vol 137 ◽  
pp. 33-49 ◽  
Author(s):  
Hong-Jiang Li ◽  
Yuan-Bo Pan ◽  
Zhao-Liang Sun ◽  
Yi-Yu Sun ◽  
Xi-Tao Yang ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Axon Regeneration ◽  
Optic Nerve Crush ◽  
Astrocyte Activation ◽  
Nerve Crush

scholarly journals B-RAF kinase drives developmental axon growth and promotes axon regeneration in the injured mature CNS

2014 ◽  
Vol 211 (5) ◽  
pp. 801-814 ◽  
Author(s):  
Kevin J. O’Donovan ◽  
Kaijie Ma ◽  
Hengchang Guo ◽  
Chen Wang ◽  
Fang Sun ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Axon Regeneration ◽  
Axon Growth ◽  
Loss Of Function ◽  
Pten Loss ◽  
Raf Kinase ◽  
Central Nervous Systems ◽  
Neurotrophin Signaling ◽  
Peripheral Sensory

Activation of intrinsic growth programs that promote developmental axon growth may also facilitate axon regeneration in injured adult neurons. Here, we demonstrate that conditional activation of B-RAF kinase alone in mouse embryonic neurons is sufficient to drive the growth of long-range peripheral sensory axon projections in vivo in the absence of upstream neurotrophin signaling. We further show that activated B-RAF signaling enables robust regenerative growth of sensory axons into the spinal cord after a dorsal root crush as well as substantial axon regrowth in the crush-lesioned optic nerve. Finally, the combination of B-RAF gain-of-function and PTEN loss-of-function promotes optic nerve axon extension beyond what would be predicted for a simple additive effect. We conclude that cell-intrinsic RAF signaling is a crucial pathway promoting developmental and regenerative axon growth in the peripheral and central nervous systems.

scholarly journals Combined inhibition of apoptosis and necrosis promotes transient neuroprotection of retinal ganglion cells and partial-axon regeneration after optic nerve damage

2018 ◽  
Author(s):  
Maki Kayama ◽  
Kumiko Omura ◽  
Yusuke Murakami ◽  
Edith Reshef ◽  
Aristomenis Thanos ◽  
...  
Keyword(s):  
Cell Death ◽  
Optic Nerve ◽  
Axonal Regeneration ◽  
Axon Regeneration ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Interacting Protein ◽  
Caspase Inhibition ◽  
Apoptosis And Necrosis

SUMMARYRetinal ganglion cell (RGC) death is the hallmark of glaucoma. Axonal injury is thought to precede RGC loss in glaucoma, and thus studies using an optic nerve (ON) crush model have been widely used to investigate mechanisms of cell death that are common to both conditions. Prior work has focused on the involvement of caspases in RGC death, but little is known about the contribution of other forms of cell death such as necrosis. In this study we show that receptor interacting protein (RIP) kinase-mediated necrosis normally plays a role in RGC death and acts in concert with caspase-dependent apoptosis. The expression of RIP3, a key activator of RIP1 kinase, as well as caspase activity, increased following ON injury. Caspase inhibition alone failed to provide substantial protection to injured RGCs and unexpectedly exacerbated necrosis. In contrast, pharmacologic or genetic inhibition of RIP kinases in combination with caspase blockade delayed both apoptotic and necrotic RGC death, although RGCs still continued to die. Furthermore, inhibition of RIP1 kinase promoted a moderate level of axon regeneration that was only minimal affected by caspase inhibition. In conclusion, multiple approaches are required for effective RGC death prevention and axonal regeneration. Further studies are needed to elucidate more effective long term strategies that can lead to sustained neuroprotection and regeneration.

Magnocellular neurosecretory axon regeneration into rat intrahypothalamic optic nerve allografts

1989 ◽  
Vol 24 (2) ◽  
pp. 163-168 ◽  
Author(s):  
H.-D. Dellmann ◽  
L.-F. Lue ◽  
S. I. Bellin ◽  
M. Quassat
Keyword(s):  
Optic Nerve ◽  
Axon Regeneration ◽  
Neurosecretory Axon
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