ArticleBMC biology2020
In vivo imaging of injured cortical axons reveals a rapid onset form of Wallerian degeneration.
Article in BMC biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Myelin sheaths persist for weeks following axon degeneration.Science advances · 2026Article
- Fusogen-induced recovery of spinal cord function and morphology after complete transection.PloS one · 2026Article
- Increased synaptic turnover in injured cortical axons: exploring the role of SARM1 ablation.Frontiers in synaptic neuroscience · 2026Article
- Impaired axon regeneration and heightened synaptic dynamics in the injured aged mammalian cortex.iScience · 2025Article
- Repetitive transcranial magnetic stimulation increases synaptic plasticity of cortical axons in the APP/PS1 amyloidosis mouse model.Neurophotonics · 2025Article
- Approaches to quantify axonal morphology for the analysis of axonal degeneration.Neural regeneration research · 2023Article
- A Brief Review of In Vitro Models for Injury and Regeneration in the Peripheral Nervous System.International journal of molecular sciences · 2022Review
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundDespite the widespread occurrence of axon and synaptic loss in the injured and diseased nervous system, the cellular and molecular mechanisms of these key degenerative processes remain incompletely understood. Wallerian degeneration (WD) is a tightly regulated form of axon loss after injury, which has been intensively studied in large myelinated fibre tracts of the spinal cord, optic nerve and peripheral nervous system (PNS). Fewer studies, however, have focused on WD in the complex neuronal circuits of the mammalian brain, and these were mainly based on conventional endpoint histological methods. Post-mortem analysis, however, cannot capture the exact sequence of events nor can it evaluate the influence of elaborated arborisation and synaptic architecture on the degeneration process, due to the non-synchronous and variable nature of WD across individual axons.
resultsTo gain a comprehensive picture of the spatiotemporal dynamics and synaptic mechanisms of WD in the nervous system, we identify the factors that regulate WD within the mouse cerebral cortex. We combined single-axon-resolution multiphoton imaging with laser microsurgery through a cranial window and a fluorescent membrane reporter. Longitudinal imaging of > 150 individually injured excitatory cortical axons revealed a threshold length below which injured axons consistently underwent a rapid-onset form of WD (roWD). roWD started on average 20 times earlier and was executed 3 times slower than WD described in other regions of the nervous system. Cortical axon WD and roWD were dependent on synaptic density, but independent of axon complexity. Finally, pharmacological and genetic manipulations showed that a nicotinamide adenine dinucleotide (NAD
conclusionsOur data illustrate how in vivo time-lapse imaging can provide new insights into the spatiotemporal dynamics and synaptic mechanisms of axon loss and assess therapeutic interventions in the injured mammalian brain.
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