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Updated: Jun 28, 2026

Two-photon Imaging of Cellular Dynamics in the Mouse Spinal Cord
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Differential changes in axonal conduction following CNS demyelination in two mouse models.

Yoshio Bando1, Kaoru Takakusaki, Shinji Ito

  • 1Department of Functional Anatomy and Neuroscience, Asahikawa Medical College, Asahikawa, Hokkaido 078-8510, Japan. ybando@asahikawa-med.ac.jp

The European Journal of Neuroscience
|November 1, 2008
PubMed
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Nerve conduction changes were studied in demyelinating mouse models. Cuprizone treatment impaired nerve conduction, while shiverer mice showed no significant changes, suggesting distinct demyelination mechanisms.

Area of Science:

  • Neuroscience
  • Demyelinating Diseases
  • Animal Models

Background:

  • Investigating molecular mechanisms of demyelinating diseases often uses transgenic and disease model mice.
  • Changes in nerve conduction in these models are less understood.
  • Demyelination affects nerve signal transmission, crucial for CNS function.

Purpose of the Study:

  • To establish an experimental system for measuring cortical neuron response latency in mice.
  • To examine changes in nerve conduction in cuprizone-induced demyelination and myelin basic protein-deficient shiverer mice.
  • To compare electrophysiological assessments with histological findings in demyelinating models.

Main Methods:

  • Established a system to measure response latency of cortical neurons via stimulating and recording electrodes in the sensori-motor cortices.

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Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
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  • Administered cuprizone to induce demyelination and assessed nerve conduction at various time points.
  • Examined response latencies in myelin basic protein-deficient shiverer mice and compared them to wild-type controls.
  • Utilized electron microscopy to confirm demyelination and remyelination in the corpus callosum.

    • Main Results:

    • Cuprizone treatment significantly increased response latency in cortical neurons, indicating impaired nerve conduction.
    • Response latency partially restored after cuprizone removal, correlating with observed remyelination.
    • Shiverer mice with myelin abnormalities showed no significant difference in response latency compared to wild-type mice.
    • Electron microscopy confirmed cuprizone-induced demyelination and subsequent remyelination.

    Conclusions:

    • Electrophysiological assessments reveal distinct effects of different demyelinating mechanisms on axon conduction.
    • Cuprizone-induced demyelination impacts nerve conduction, while myelin defects in shiverer mice do not significantly alter it.
    • This study provides new insights into the pathophysiology of demyelination in CNS animal models.