# An electro-mechanical mechanism of spike propagation in myelinated axons

> **NIH NIH R21** · UNIVERSITY OF CALIFORNIA BERKELEY · 2021 · $440,687

## Abstract

Nerve cells send electrical impulses down long fibers called axons. Many axons are
surrounded with a layer of insulation called the myelin sheath, a structure that ensures
that the impulses propagate very rapidly and reliably. Tiny gaps in the sheath, called
nodes of Ranvier, serve to amplify the electrical impulses, driving them forward to the
end of the axon, where chemical signals are sent to other neurons or muscle cells at
structures called synapses. In multiple sclerosis (MS) and other demyelinating diseases
the myelin sheath is damaged and the nodes of Ranvier are disrupted, slowing or even
stopping the electrical impulses from reaching the synapse. Our aim is to test a new idea
that could fundamentally change our understanding of how electrical impulses are
amplified at nodes and how they travel so fast along axons. Instead of the amplification
mechanism being purely electrical, we propose a new mechanism, in which physical
swelling of the node along a novel molecule that senses swelling, are crucial for amplifying
electrical impulses, causing them to propagate faster and more reliably. This idea was
spawned by the recent discovery that a specialized mechanically-sensitive ion channel
named TRAAK is highly concentrated at nodes. TRAAK is a potassium channel, which are
already known to be important for shaping electrical impulses. The presence of TRAAK
at nodes raises the possibility that it serves a key electro-mechanical function. This
exploratory/developmental project will answer 3 key questions: 1) To what extent do
electrical impulses cause swelling of nodes of Ranvier in the brain? 2) Are TRAAK
channels necessary for proper electrical impulse propagation in myelinated axon in the
brain? 3) Can optical manipulation of a genetically-engineered photo-controlled version
of TRAAK restore proper spike propagation in myelinated axons in the brain? Results
gleaned from this work will be of great importance for understanding fundamental
physiological processes necessary for normal function of the nervous system. These
findings will provide new insights into events that occur in demyelinating diseases such
as MS, and may lead to new treatment strategies, including the development of drugs for
mitigating their debilitating symptoms.

## Key facts

- **NIH application ID:** 10194107
- **Project number:** 1R21NS121431-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA BERKELEY
- **Principal Investigator:** RICHARD H KRAMER
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $440,687
- **Award type:** 1
- **Project period:** 2021-04-01 → 2023-09-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10194107

## Citation

> US National Institutes of Health, RePORTER application 10194107, An electro-mechanical mechanism of spike propagation in myelinated axons (1R21NS121431-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10194107. Licensed CC0.

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