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The Fibular Nerve Injury Method: A Reliable Assay to Identify and Test Factors That Repair Neuromuscular Junctions
Published on: August 11, 2016
Mice lacking basic fibroblast growth factor showed faster sensory recovery
Julia Jungnickel1, Kirsten Haastert, Martin Grzybek
1Hannover Medical School, Institute of Neuroanatomy, Germany. jungnickel.julia@mh-hannover.de
Experimental Neurology
|June 13, 2009
Summary
Basic fibroblast growth factor (FGF-2) deficiency accelerates mechanosensory recovery after sciatic nerve injury by enhancing axon and myelin structure. Loss of FGF-2 transiently improves nerve repair structural restoration.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Molecular Biology
Background:
- Neurotrophic factors are crucial for peripheral nerve repair.
- Basic fibroblast growth factor (FGF-2) is upregulated post-nerve injury and regulates Schwann cell proliferation.
- FGF-2 plays a role in axonal maturation and remyelination.
Purpose of the Study:
- To investigate the functional impact of FGF-2 deficiency on sensory and motor nerve recovery after sciatic nerve crush.
- To elucidate the role of FGF-2 in the structural recovery of peripheral nerves.
Main Methods:
- Sciatic nerve crush injury model in FGF-2 deficient and wild-type mice.
- Functional assessments including pinch test, walking track analysis, and rotarod test.
- Histological and molecular analyses of nerve regeneration at 2 and 4 weeks post-injury.
Main Results:
- FGF-2 deficient mice showed faster recovery of mechanosensory function but not motor function.
- Two weeks post-injury, mutant mice exhibited increased axon and myelin size without changes in fiber numbers.
- Absence of FGF-2 led to significantly enhanced expression of myelin protein zero in lesioned nerves.
Conclusions:
- Loss of FGF-2 positively influences mechanosensory function recovery.
- FGF-2 deficiency transiently accelerates structural recovery, including increased axon and myelin size.
- Enhanced myelin protein zero expression in FGF-2 deficient mice suggests a role in accelerated remyelination.
