AI Article Synopsis
- The study investigates the role of protease-activated receptor-2 (PAR-2) in pain processing within sensory neurons, particularly how it influences nociceptive signaling.
- The researchers found that both a specific PAR-2 agonist and a control peptide induced the expression of spinal Fos, a nociception marker, in naive rats, but only the PAR-2 agonist triggered this response in mast cell-depleted rats.
- They concluded that activation of spinal nociceptive neurons can occur via peripheral PAR-2 activation and that this process is partly mediated by protein kinase C (PKC), as indicated by the blocking effect of certain inhibitors.
Article Abstract
Protease-activated receptor-2 (PAR-2) in the sensory neurons may be involved in nociceptive processing. We attempted to detect and characterize specific expression of spinal Fos, a marker of nociception, in mast cell-depleted rats. Intraplantar (i.pl.) administration of not only the PAR-2 agonist SLIGRL-NH2, but also the control peptide LSIGRL-NH2, induced Fos expression in naive rats, whereas only the former specifically produced Fos expression in mast cell-depleted rats. This Fos expression was blocked by intrathecal DAMGO, a mu-opioid agonist, and, in part, by i.pl. calphostin C, a protein kinase C (PKC) inhibitor. Thus, specific expression of spinal Fos following peripheral PAR-2 activation is detectable in mast cell-depleted rats, suggesting activation of spinal nociceptive neurons, which is partially mediated by activation of PKC.
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| http://dx.doi.org/10.1097/00001756-200203250-00031 | DOI Listing |
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