In the inflammatory pain, P2X-type purinergic receptors which are activated by extracellular ATP can have either direct action on nociceptors by activate and sensitize them and indirectly leading to the release of inflammatory mediators that, in turn, are able to sensitize nociceptors. There are two types of purinergic receptors that seem to be most important for the inflammatory pain development: the P2X2 and P2X2/3 receptors present in nociceptors and P2X7 receptors present in immune and glial cells. Although there are several studies describing the function of neuronal receptors, it is not known the role of P2X7 receptors present in glial cells derived from the sensory ganglia, called satellite cells. Recent studies indicate that activation of P2X7 receptors induced by ATP is an essential step in maturation and release of IL-1², a proinflammatory cytokine in peripheral tissue. In the case of inflammatory pain, IL-1² has particular importance since it is responsible for activating cyclooxygenases enzymes (Cox-1 and Cox-2) that will produce prostanoids capable of sensitizing nociceptors. It is known that peripheral tissue inflammation leads to IL-1² production in sensory ganglia. Recently, our group demonstrated Cox increase in sensory ganglia and the subsequent prostaglandins synthesis and release are essential for sensitization of nociceptive primary neurons during peripheral tissue inflammation Therefore, the hypothesis to be tested in this project is that during peripheral tissue inflammation ATP is released from the cell bodies of primary sensory neurons and this ATP, through activation of P2X7 receptors present in satellite cells, will promote the release of IL -1² on dorsal root ganglia, contributing to nociceptors sensitization.
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