ArticleExperimental neurology2013
Dorsal column sensory axons degenerate due to impaired microvascular perfusion after spinal cord injury in rats.
Article in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- The emerging role of cuproptosis in spinal cord injury.Frontiers in immunology · 2025Review
- Applications of Stem Cell-Derived Extracellular Vesicles in Nerve Regeneration.International journal of molecular sciences · 2024Review
- Trigeminal nerve stimulation: a current state-of-the-art review.Bioelectronic medicine · 2023Review
- Neuron-Derived Exosomes Promote the Recovery of Spinal Cord Injury by Modulating Nerve Cells in the Cellular Microenvironment of the Lesion Area.Molecular neurobiology · 2023Article
- Mitochondrial function in spinal cord injury and regeneration.Cellular and molecular life sciences : CMLS · 2022Review
- Clemastine Enhances Myelination, Delays Axonal Loss and Promotes Functional Recovery in Spinal Cord Injury.Neurochemical research · 2022Article
- Microtubule Stabilization Promotes Microcirculation Reconstruction After Spinal Cord Injury.Journal of molecular neuroscience : MN · 2021Article
- M2 Macrophages Promote PDGFRβFrontiers in pharmacology · 2021Article
- Retracted Article: Melatonin protects spinal cord injury by up-regulating IGFBP3 through the improvement of microcirculation in a rat model.RSC advances · 2019Article
- The Biology of Regeneration Failure and Success After Spinal Cord Injury.Physiological reviews · 2018Review
- Reduced FAK-STAT3 signaling contributes to ER stress-induced mitochondrial dysfunction and death in endothelial cells.Cellular signalling · 2017Article
- Melatonin prevents blood vessel loss and neurological impairment induced by spinal cord injury in rats.The journal of spinal cord medicine · 2017Article
- Intrathecal Acetyl-L-Carnitine Protects Tissue and Improves Function after a Mild Contusive Spinal Cord Injury in Rats.Journal of neurotrauma · 2016Article
- Does being female provide a neuroprotective advantage following spinal cord injury?Neural regeneration research · 2015Review
- Recent advances in the pharmacologic treatment of spinal cord injury.Metabolic brain disease · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms contributing to axon loss after spinal cord injury (SCI) are largely unknown but may involve microvascular loss as we have previously suggested. Here, we used a mild contusive injury (120 kdyn IH impactor) at T9 in rats focusing on ascending primary sensory dorsal column axons, anterogradely traced from the sciatic nerves. The injury caused a rapid and progressive loss of dorsal column microvasculature and oligodendrocytes at the injury site and penumbra and an ~70% loss of the sensory axons by 24 h. To model the microvascular loss, focal ischemia of the T9 dorsal columns was achieved via phototoxic activation of intravenously injected rose bengal. This caused an ~53% loss of sensory axons and an ~80% loss of dorsal column oligodendrocytes by 24 h. Axon loss correlated with the extent and axial length of microvessel and oligodendrocyte loss along the dorsal column. To determine if oligodendrocyte loss contributes to axon loss, the glial toxin ethidium bromide (EB; 0.3 μg/μl) was microinjected into the T9 dorsal columns, and resulted in an ~88% loss of dorsal column oligodendrocytes and an ~56% loss of sensory axons after 72 h. EB also caused an ~75% loss of microvessels. Lower concentrations of EB resulted in less axon, oligodendrocyte and microvessel loss, which were highly correlated (R(2) = 0.81). These data suggest that focal spinal cord ischemia causes both oligodendrocyte and axon degeneration, which are perhaps linked. Importantly, they highlight the need of limiting the penumbral spread of ischemia and oligodendrocyte loss after SCI in order to protect axons.
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