Sodium Channel Nav1.6 and Nerve Injury
Author Information
Author(s): Henry Michael A, Freking Angelique R, Johnson Lonnie R, Levinson S Rock
Primary Institution: University of Colorado at Denver and Health Sciences Center
Hypothesis
The study evaluates the role of the sodium channel isoform Nav1.6 in the remodeling of sodium channels following infraorbital nerve injury.
Conclusion
Nav1.6 is involved in the remodeling of sodium channels at nodal sites after nerve injury, which may affect the excitability of myelinated axons in pain models.
Supporting Evidence
- Nav1.6 accumulations were significantly larger and denser in lesioned IONs compared to normal IONs.
- The average size of Nav1.6 accumulations was greater in lesioned IONs.
- Immunofluorescence intensity of Nav1.6 was significantly higher in lesioned IONs.
Takeaway
When a nerve gets hurt, a special protein called Nav1.6 gets bigger and changes shape, which might make the nerve more sensitive to pain.
Methodology
The study used confocal microscopy to analyze the size and density of Nav1.6 accumulations in normal and lesioned infraorbital nerves.
Limitations
The study did not differentiate between effects of axotomy and chromic suture on sodium channel remodeling.
Participant Demographics
Four young adult female Sprague-Dawley rats were used as experimental subjects.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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