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Updated: Jul 28, 2026
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In Vivo Intracellular Recording of Type-Identified Rat Spinal Motoneurons During Trans-Spinal Direct Current Stimulation
Published on: May 11, 2020
Low intensity spinal cord stimulation may induce cutaneous vasodilation via CGRP release
S Tanaka1, K W Barron, M J Chandler
1Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190, USA.
Brain Research
|March 30, 2001
Summary
Spinal cord stimulation (SCS) below motor threshold causes skin blood vessel dilation. This vasodilation is mediated by calcitonin gene-related peptide (CGRP) release from sensory nerves, not sympathetic inhibition.
Area of Science:
- Neuroscience
- Physiology
Background:
- Spinal cord stimulation (SCS) is used clinically for pain management.
- The precise mechanisms underlying SCS-induced vasodilation, particularly at sub-motor threshold intensities, remain incompletely understood.
- Investigating SCS effects on peripheral vasculature is crucial for optimizing therapeutic applications.
Purpose of the Study:
- To determine the mechanism of cutaneous vasodilation induced by SCS below motor threshold (MT).
- To differentiate between sympathetic inhibition and sensory nerve activation as SCS effectors.
- To identify the key signaling molecules involved in SCS-mediated vasodilation.
Main Methods:
- Anesthetized rats were subjected to SCS using clinically relevant parameters (50 Hz, 0.2 ms) at varying intensities (30%, 60%, 90% MT).
- Cutaneous vasodilation was measured.
- Pharmacological agents, including hexamethonium (ganglion blocker) and CGRP-(8-37) (CGRP receptor antagonist), were used to probe the underlying pathways.
Main Results:
- SCS induced significant cutaneous vasodilation.
- The observed vasodilation was unaffected by hexamethonium, ruling out sympathetic ganglion involvement.
- SCS-induced vasodilation was completely blocked by CGRP-(8-37), indicating a critical role for CGRP.
Conclusions:
- SCS at sub-motor threshold intensities triggers cutaneous vasodilation.
- The primary mechanism involves the antidromic activation of sensory nerve fibers.
- Calcitonin gene-related peptide (CGRP) release from activated sensory nerves mediates the observed vasodilation.
