ArticleCellular and molecular neurobiology2025
A Focal Traumatic Injury to the Neonatal Rodent Spinal Cord Causes an Immediate and Massive Spreading Depolarization Sustained by Chloride Ions, with Transient Network Dysfunction.
Article in Cellular and molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Immediate cortical glial alterations following spinal cord injury: Evidence from a novel in vitro model.Experimental physiology · 2026Article
- Immediate Consequences of a Spinal Cord Injury During Development: Unique Insights From Ex Vivo Models.Neural plasticity · 2026Review
- Acute intermittent hypoxia in neonatal rodent central nervous system facilitates respiratory frequency through the recruitment of hypothalamic areas.Experimental physiology · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
In clinics, physical injuries to the spinal cord cause a temporary motor areflexia below lesion, known as spinal shock. This topic is still underexplored due to the lack of preclinical spinal cord injury (SCI) models that do not use anesthesia, which would affect spinal excitability. Our innovative design considered a custom-made micro impactor that provides localized and calibrated strikes to the ventral surface of the thoracic spinal cord of the entire CNS isolated from neonatal rats. Before and after injury, multiple ventral root (VR) recordings continuously traced respiratory rhythm, baseline spontaneous activities, and electrically induced reflex responses. As early as 200 ms after the lowering of the impactor, an immediate transient depolarization spread from the injury site to the whole spinal cord with distinct segmental velocities. Stronger strikes induced higher potentials causing, close by the site of injury, a transient drop in spinal cord oxygenation (SCO
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