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Related Experiment Videos

Blood-spinal cord barrier response to transection.

L J Noble, D S Maxwell

    Experimental Neurology
    |January 1, 1983
    PubMed
    Summary

    The blood-spinal cord barrier (BSB) integrity is compromised after surgery, with tracers detected in neural tissue. While barrier function recovers within a day, enhanced endothelial cell activity persists for up to seven days.

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    Area of Science:

    • Neuroscience
    • Cell Biology
    • Physiology

    Background:

    • The blood-spinal cord barrier (BSB) protects the spinal cord from harmful substances.
    • Surgical spinal cord transection can disrupt the BSB's integrity.
    • Understanding BSB permeability is crucial for spinal cord injury research.

    Purpose of the Study:

    • To evaluate the integrity of the blood-spinal cord barrier (BSB) distal to a surgical transection.
    • To investigate the time course of BSB permeability changes after injury.

    Main Methods:

    • Utilized light and electron microscopy to assess BSB integrity.
    • Employed tracers Evans blue albumin (EBA) and horseradish peroxidase (HRP) to detect leakage.
    • Examined endothelial cell transport mechanisms, including pinocytosis and vesicular transport.

    Main Results:

    • Evans blue albumin (EBA) fluorescence was observed up to 0.45 mm distal to the transection.
    • Tracer uptake by neurons and glial cells, and leakage from intrinsic vessels were noted.
    • Ultrastructural analysis revealed pinocytosis and vesicular transport in endothelial cells, with limited tight junction leakage.
    • BSB selectivity appeared restored after 1 day, with no vesicular transport of HRP.
    • Enhanced endothelial pinocytosis persisted for up to 7 days post-injury.

    Conclusions:

    • Surgical transection causes transient but significant disruption of the blood-spinal cord barrier.
    • The BSB demonstrates remarkable recovery of selectivity within 24 hours.
    • Persistent alterations in endothelial cell transport mechanisms suggest ongoing cellular responses to injury.

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