Motor Function Assessment
Objective: Evaluation of motor deficits and functional impairments in mice following spinal cord injury with and without reactive astrocyte ablation
This is a Motor Function Assessment protocol using mouse as the model organism. The procedure involves 3 procedural steps, 1 materials. Extracted from a 2004 paper published in Journal of Neuroscience.
Model and subjects
mouse • transgenic mice expressing glial fibrillary acid protein-herpes simplex virus-thymidine kinase transgene and nontransgenic control mice • unknown • Not specified • Not specified
Study window
Estimated timing pending
Core workflow
Spinal Cord Injury Induction • Ganciclovir Treatment • Motor Function Assessment
Primary readouts
- Motor deficits severity
- Functional impairment reversibility
- Blood-brain barrier integrity
- Leukocyte infiltration
Key equipment and reagents
Verified items
0
Direct vendor links
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Protocol Steps
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Spinal Cord Injury Induction
Mice received either small stab injuries or moderate crush injuries to the spinal cord
Note: Two injury types were tested: small stab injuries and moderate crush injuries
View evidence from paper
“Mice expressing a glial fibrillary acid protein-herpes simplex virus-thymidine kinase transgene were given mild or moderate SCI”
Ganciclovir Treatment
Transgenic mice were treated with ganciclovir to ablate reactive astrocytes in the immediate vicinity of the spinal cord injury
Note: Treatment applied to transgenic mice only; control mice did not receive GCV
View evidence from paper
“treated with the antiviral agent ganciclovir (GCV) to ablate dividing, reactive, transgene-expressing astrocytes in the immediate vicinity of the SCI”
Motor Function Assessment
Motor deficits and functional impairments were evaluated in both control and transgenic mice following spinal cord injury
Note: Assessment conducted in mice with small stab injuries and moderate crush injuries, with and without astrocyte ablation
View evidence from paper
“Small stab injuries in control mice caused little tissue disruption, little demyelination, no obvious neuronal death, and mild, reversible functional impairments”