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The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice
Published on: July 16, 2014
Algesic agents exciting muscle nociceptors
1Department of Anatomy and Cell Biology III, Heidelberg University, Im Neuenheimer Feld 307, 69120 Heidelberg, Germany. mense@ana.uni-heidelberg.de
Experimental Brain Research
|January 14, 2009
Summary
Muscle pain arises from specific chemical stimuli like low pH and adenosine triphosphate (ATP). While these activate nerve endings, inflammation can reduce their effectiveness in signaling pain.
Area of Science:
- Neuroscience
- Pain Research
- Muscle Physiology
Background:
- Muscle nociceptors are free nerve endings transmitting pain signals via myelinated (group III) and unmyelinated (group IV) fibers.
- Approximately 40% of muscle nociceptors have low mechanical thresholds, suggesting non-nociceptive roles.
- Acidic interstitial pH (lowering tissue pH) and released adenosine triphosphate (ATP) are key chemical stimuli causing muscle pain.
Purpose of the Study:
- To investigate the role of chemical stimuli in muscle pain.
- To understand how inflammation affects the sensitivity of muscle nociceptors to chemical stimuli.
- To identify specific chemical agents that exclusively activate nociceptive pathways.
Main Methods:
- Morphological characterization of muscle nociceptors.
- Investigation of chemical stimuli (low pH, ATP) and their effects on nerve endings.
- Assessment of desensitizing agents like capsaicin, brain-derived neurotrophic factor, and tumor necrosis factor-alpha.
- Experimental induction of chronic muscle inflammation in rats using complete Freund's adjuvant.
- Evaluation of the effectiveness of ATP, nerve growth factor (NGF), and low pH in inflamed muscle.
Main Results:
- Low pH and ATP are significant stimuli for muscle pain, playing a lesser role in cutaneous pain.
- Substances like capsaicin, brain-derived neurotrophic factor, and tumor necrosis factor-alpha can desensitize mechanosensitive group IV receptors.
- Nerve growth factor (NGF) is identified as a substance that exclusively excites nociceptive group IV receptors.
- In chronically inflamed rat muscle, common pain stimuli (ATP, NGF, low pH) were less effective.
- Increased concentrations of ATP, NGF, and H+ in inflamed muscle may explain the reduced effectiveness of experimental administration.
Conclusions:
- Muscle pain involves specific chemical signaling pathways distinct from cutaneous pain.
- Inflammation alters the responsiveness of muscle nociceptors to chemical stimuli.
- Nerve growth factor (NGF) represents a unique activator of nociceptive pathways in muscle.
- The paradoxical reduced sensitivity to stimuli in inflamed muscle suggests complex regulatory mechanisms.
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