Axonal Degeneration
Axonal Degeneration - Related Videos
04:49
Two-Photon Laser-Induced Neural Injury: A Method to Observe Axon Degeneration and Regeneration in Drosophila Larvae
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2023
This video describes two-photon laser ablation of axons in a Drosophila melanogaster larva and an example protocol to induce injury and image the injury site.
08:36
A Versatile Murine Model of Subcortical White Matter Stroke for the Study of Axonal Degeneration and White Matter Neurobiology
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Cited by 21 •
2016
Here we present methodology for the production of a focal stroke in murine white matter by local injection of an irreversible endothelial nitric oxide synthase (eNOS) inhibitor (L-Nio). Presented are two stereotactic variations, retrograde neuronal tracing, and fresh tissue labeling and dissection that expand the potential applications of this technique.
09:25
Laser Nanosurgery of Cerebellar Axons In Vivo
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Cited by 7 •
2014
Two-photon imaging, coupled to laser nanodissection, are useful tools to study degenerative and regenerative processes in the central nervous system with subcellular resolution. This protocol shows how to label, image, and dissect single climbing fibers in the cerebellar cortex in vivo.
06:40
Screening of Axonal Degeneration in Carpal Tunnel Syndrome Using Ultrasonography and Nerve Conduction Studies
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Cited by 5 •
2019
Here we present a protocol using nerve conduction studies and ultrasound to screen potential axonal degeneration associated with carpal tunnel syndrome. The criteria for differentiation are established. Compared to conventional approaches, this method is noninvasive, convenient, and efficient, with an overall satisfactory accuracy, sensitivity, and specificity.
02:40
Axonal Regeneration in the Sciatic Nerve of a Mouse Following a Crush Injury
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2025
Source: Li, Q., et al. Investigating Mammalian Axon Regeneration: In Vivo Electroporation of Adult Mouse Dorsal Root Ganglion. J. Vis. Exp. (2018)This video demonstrates the process of axonal regeneration in a mouse sciatic nerve following a crush injury. The isolated nerve is fixed and prepared for imaging, with fluorescent proteins expressed in neurons to visualize axon growth. Using an epifluorescence microscope, axon regeneration is traced from the injury site to assess the extent of...
FAQs
Loss of essential transport can deprive distant axonal regions of materials or signals needed for maintenance. The resulting failure is linked to disrupted energy metabolism, making the axon more vulnerable to calcium influx and protease activation. Tracking transport and metabolic disruption helps researchers connect an initiating injury with later structural breakdown and impaired neural connectivity.
Calcium influx acts as a damaging signal that can activate proteases such as calpain. These enzymes contribute to the breakdown of the axonal cytoskeleton, the internal structural framework that supports axon integrity. This connection explains how an initial disturbance in axonal physiology can progress into fragmentation and provides a mechanistic target for studies of secondary damage.
Calpain helps convert biochemical stress into structural injury. Once activated in association with calcium influx, this protease contributes to cytoskeletal disassembly, weakening the axon’s internal organization and promoting fragmentation. Because calpain links altered calcium regulation with visible axonal breakdown, it is an important component when investigators analyze mechanisms of nervous system injury.
Wallerian degeneration provides a framework for examining what happens to axonal segments after damage or loss of essential support. Studying this process connects the original injury with cytoskeletal disassembly, fragmentation, and eventual glial clearance. It is therefore useful for understanding how peripheral nerve injury can disrupt neural connectivity beyond the site of the initial insult.
A useful investigation can follow the progression from axonal damage or transport loss to disrupted energy metabolism, calcium influx, calpain activation, cytoskeletal disassembly, and fragmentation. The later response includes clearance by glial cells. Examining these linked stages helps distinguish initiating events from downstream structural outcomes and clarifies where protective interventions might act.
Biomarkers can help indicate that axonal injury or degeneration is occurring and can support comparisons between disease, injury, or toxic exposure contexts. The source material identifies biomarker development as a research direction linked to these mechanisms. Such indicators may help evaluate axon preservation, secondary damage, or responses to approaches intended to promote nerve regeneration.
Mechanistic studies support three broad therapeutic goals: preserving vulnerable axons, limiting secondary damage, and promoting nerve regeneration. These aims reflect different points in the degenerative sequence, from preventing further structural loss to improving recovery after injury. The same framework is relevant to peripheral nerve injuries, neurodegenerative disorders, and toxic exposures that impair neural connectivity.