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Related Experiment Video

Updated: May 20, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Long-term nerve excitability changes by persistent Na+ current blocker ranolazine.

Hiroyuki Nodera¹, Seward B Rutkove

¹Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, USA. hnodera@clin.med.tokushima-u.ac.jp

Neuroscience Letters

|July 25, 2012

Summary

Chronic blockade of persistent sodium current (Na(p)) using ranolazine in mice reduced nerve excitability. This suggests potential for treating neuropathic pain and neurodegenerative diseases.

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Area of Science:

Neuroscience
Pharmacology
Physiology

Background:

Persistent sodium current (Na(p)) in peripheral axons is crucial for axonal excitability.
Abnormal Na(p) is implicated in neurodegeneration and neuropathic pain, making it a therapeutic target.

Purpose of the Study:

To evaluate the chronic effects of selective Na(p) blockade on axonal excitability in vivo.
To assess ranolazine's potential as a long-term therapeutic agent for peripheral nerve conditions.

Main Methods:

Axonal excitability testing was conducted in normal male mice.
Mice received daily intraperitoneal injections of ranolazine (50mg/kg) for one week.
Tail sensory nerve action potentials (SNAPs) were recorded to assess nerve excitability.

Main Results:

Ranolazine treatment significantly decreased the strength-duration time constant compared to controls (P<0.03).
This observed change is attributed to the sustained effects of ranolazine on Na(p).
Ranolazine did not affect other ion channels influencing axonal excitability.

Conclusions:

Chronic Na(p) blockade with ranolazine alters axonal excitability through sustained effects.
Further research is warranted to explore chronic Na(p) blockade as a therapeutic strategy for peripheral nerve diseases characterized by abnormal excitability.