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Inflammation-induced changes in peripheral glutamate receptor populations
1Department of Anatomy and Neurosciences, Marine Biomedical Institute, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-1069, USA. smcarlto@utmb.edu
Brain Research
|February 19, 1999
Summary
Inflammation increases the number of sensory axons expressing ionotropic glutamate receptors, including N-methyl-d-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainate (KA) receptors. This suggests a role in peripheral pain sensitization.
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- Ionotropic glutamate receptors (NMDA, AMPA, KA) are found on sensory axons in normal skin.
- Activation of these receptors is linked to nociception and inflammatory pain.
Purpose of the Study:
- To investigate the role of ionotropic glutamate receptors in peripheral hypersensitivity during inflammation.
- To quantify changes in NMDA, AMPA, and KA receptor expression in sensory axons following induced inflammation.
Main Methods:
- Complete Freund's adjuvant (CFA) was used to induce inflammation in animal models.
- Immunohistochemical labeling was performed on cutaneous nerves from inflamed and non-inflamed paws.
- Proportions of unmyelinated and myelinated axons expressing NMDA, AMPA, and KA receptors were quantified.
Main Results:
- Significant increases in the proportions of unmyelinated axons expressing NMDA (61% vs 48%), AMPA (43% vs 22%), and KA (48% vs 27%) receptors were observed in inflamed paws compared to non-inflamed paws.
- Significant increases in the proportions of myelinated axons expressing NMDA (61% vs 43%), AMPA (61% vs 42%), and KA (43% vs 28%) receptors were also found in inflamed paws.
- These changes were statistically significant, indicating an upregulation of glutamate receptors during inflammation.
Conclusions:
- The number of sensory axons containing ionotropic glutamate receptors increases during inflammation.
- This increase in receptor expression may contribute to the development of peripheral sensitization and hypersensitivity in inflammatory pain states.