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Updated: Jun 15, 2026
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Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats
Published on: January 21, 2020
Eccentric muscle contraction and stretching evoke mechanical hyperalgesia and modulate CGRP and P2X(3) expression in
Dean Dessem1, Ranjinidevi Ambalavanar, Melena Evancho
1Department of Neural and Pain Sciences, University of Maryland, 650 West Baltimore Street, Baltimore, MD 21201, USA Graduate Program in Neuroscience, University of Maryland, Baltimore, MD, USA Department of Obstetrics and Gynecology, University of Texas, Galveston, TX 77555, USA.
Pain
|March 9, 2010
Summary
Movement and muscle damage, like eccentric contractions (EC) and stretching, cause pain and inflammation. These actions alter nerve signaling molecules, potentially increasing sensitivity to future muscle injury.
Area of Science:
- Muscle physiology
- Pain research
- Neuroscience
Background:
- Muscle pain and injury are common, impacting quality of life.
- Understanding the mechanisms of movement-induced muscle pain is crucial for developing effective treatments.
- Non-invasive models are needed to study muscle pain pathophysiology.
Purpose of the Study:
- To investigate the effects of eccentric contractions (EC) and muscle stretching on muscle pain and associated molecular changes in rats.
- To differentiate the roles of muscle contraction versus stretching in inducing pain and altering neural signaling.
- To explore the involvement of specific inflammatory mediators and neuronal markers in movement-induced muscle pain.
Main Methods:
- Induced eccentric contractions (EC) and muscle stretching in rat masseter muscles.
- Assessed muscle damage, plasma extravasation, and inflammatory cytokine levels (IL-1beta, TNF-alpha, IL-6).
- Quantified immune cell infiltration (neutrophils, macrophages) and neuropeptide expression (CGRP, P2X3) in muscle and trigeminal ganglia.
Main Results:
- Both EC and stretching caused muscle damage and inflammation.
- EC led to increased pro-inflammatory cytokines, immune cell infiltration, and mechanical hyperalgesia.
- EC and stretching upregulated P2X3 mRNA and increased P2X3-expressing neurons, suggesting enhanced nociceptor responsiveness.
Conclusions:
- Movement-based muscle damage, including EC and stretching, triggers distinct inflammatory and neural responses.
- Sustained P2X3 expression following EC and stretching may sensitize nociceptors to subsequent muscle damage.
- These findings provide insights into the mechanisms of muscle pain relevant to repeated injury.
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