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Aging-associated changes in motor axon voltage-gated Na(+) channel function in mice
Mihai Moldovan1, Mette Romer Rosberg2, Susana Alvarez2
1Department of Neuroscience and Pharmacology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Clinical Neurophysiology, Rigshospitalet, Copenhagen, Denmark.
Neurobiology of Aging
|March 1, 2016
Summary
Aging impairs motor axon function due to changes in myelin and increased Nav1.8 sodium channels. This study reveals how these age-related alterations affect nerve conduction and excitability in wild-type mice.
Area of Science:
- Neuroscience
- Aging research
- Peripheral nerve physiology
Background:
- Peripheral nerves undergo myelin abnormalities and conduction slowing with age.
- Myelin protein P0 deficiency causes severe damage and ectopic Nav1.8 expression, worsening functional impairment.
Purpose of the Study:
- To investigate the impact of aging on motor axon function, focusing on Nav1.8 expression.
- To compare nerve conduction and excitability in mature and aged wild-type mice.
Main Methods:
- Threshold tracking to measure tibial nerve conduction and excitability.
- Immunohistochemistry to assess Nav1.8 expression.
- Modeling to analyze motor fiber properties.
Main Results:
- Aged mice showed attenuated threshold electrotonus deviations, increased resting current-threshold slope, and enhanced early refractoriness.
- Modeling suggested depolarization of motor fibers in aged mice, beyond passive membrane changes.
- Increased Nav1.8 expression was observed in aged wild-type mice.
- Nav1.8 null mice lacked these depolarizing excitability features, which were reversed by a Nav1.8 blocker in aged wild-type mice.
Conclusions:
- Altered voltage-gated sodium channel isoform expression, specifically Nav1.8, contributes to age-related changes in motor axon function.
- Nav1.8 plays a significant role in the functional impairments observed in aging peripheral nerves.
