How Sodium Channel Nav1.8 Affects Action Potential in Pain Neurons
Author Information
Author(s): Patrick Harty, Stephen G. Waxman
Primary Institution: Yale University School of Medicine
Hypothesis
The presence of Nav1.8 should shift the voltage-dependence of action potential amplitude in a depolarized direction.
Conclusion
The presence of Nav1.8 allows action potential amplitude to be maintained in DRG neurons even when depolarized within the dorsal horn.
Supporting Evidence
- The study found that action potential amplitude decreases as the membrane potential is depolarized.
- Nav1.8 channels contribute significantly to maintaining action potential amplitude in DRG neurons.
- Transfection of Nav1.8 into Nav1.8(-/-) neurons restored the voltage-dependence of action potential amplitude.
Takeaway
This study shows that a special sodium channel helps pain-sensing neurons send signals even when they are under stress from high potassium levels.
Methodology
The study involved culturing small DRG neurons from mice and analyzing action potential amplitude in response to changes in membrane potential.
Participant Demographics
Adult wild type and Nav1.8(-/-) mice were used for the study.
Digital Object Identifier (DOI)
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