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Activation of p38 mitogen-activated protein kinase in spinal microglia is a critical link in inflammation-induced
Camilla I Svensson1, Martin Marsala, Anna Westerlund
1Department of Anesthesiology, University of California, San Diego, La Jolla, California, USA. csvensson@ucsd.edu
Abstract:
We examined the effect of p38 mitogen-activated protein kinase (MAPK) inhibitors in models of nociception and correlated this effect with localization and expression levels of p38 MAPK in spinal cord. There was a rapid increase in phosphorylated p38 MAPK in spinal cord following intrathecal administration of substance P or intradermal injection of formalin. Immunocytochemistry revealed that phosphorylated p38 MAPK-immunoreactive cells were predominantly present in laminae I-IV of the dorsal horn. Double-staining with markers for neurons, microglia, astrocytes and oligodendrocytes unexpectedly revealed co-localization with microglia but not with neurons or other glia. Pretreatment with p38 MAPK inhibitors (SB20358 or SD-282) had no effect on acute thermal thresholds. However, they attenuated hyperalgesia in several nociceptive models associated with spinal sensitization including direct spinal activation (intrathecal substance P) and peripheral tissue inflammation (intraplantar formalin or carrageenan). Spinal sensitization, manifested by enhanced expression of cyclo-oxygenase-2 and inflammation-induced appearance of Fos-positive neurons, was blocked by pretreatment, but not post-treatment, with p38 MAPK inhibitors. Taken together, these results indicate that spinal p38 MAPK is involved in inflammation-induced pain and that activated spinal microglia play a direct role in spinal nociceptive processing.
Insights
p38 mitogen-activated protein kinase (MAPK) inhibitors reduced pain in models of spinal sensitization. Activated spinal microglia, not neurons, play a role in processing inflammation-induced pain signals.
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- p38 mitogen-activated protein kinase (MAPK) is implicated in pain signaling.
- Its role in spinal nociception, particularly in relation to microglia, requires further elucidation.
Purpose of the Study:
- To investigate the role of spinal p38 MAPK in nociception and spinal sensitization.
- To determine the cellular localization of activated p38 MAPK in the spinal cord.
Main Methods:
- Utilized p38 MAPK inhibitors (SB20358, SD-282) in rodent models of nociception.
- Assessed pain thresholds and hyperalgesia.
- Employed immunocytochemistry and double-staining to identify cell types expressing phosphorylated p38 MAPK in the spinal cord.
Main Results:
- Phosphorylated p38 MAPK increased in the spinal cord after noxious stimuli and co-localized with microglia in the dorsal horn.
- p38 MAPK inhibitors attenuated hyperalgesia in models of spinal sensitization but not acute pain.
- Inhibitor pretreatment blocked spinal sensitization markers (COX-2, Fos) but post-treatment did not.
Conclusions:
- Spinal p38 MAPK activation is crucial for inflammation-induced hyperalgesia and spinal sensitization.
- Activated microglia in the spinal cord are key players in processing pain signals during inflammation.
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