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This can occur due to increased responsiveness of pain neurons or because of lowered activation thresholds of nociceptors, which for example occurs in TRPV1 when protons lower the heat activation threshold. Figure 1.2 shows how, when exposed to products of injury and inflammation, a variety of intracellular signaling pathways alter the sensitivity of the TRPV1 receptor (named VR1 in the diagram). For example, protons and lipid metabolites such as anandamide (AEA) released during tissue acidosis potentate VR1 activation by heat, and NGF and bradykinin bind to cell surface receptors stimulating phospholipase C signaling pathways, which are also known to enhance nociceptor excitability (Julius and Basbaum, 2001)...
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