5- Conclusion
In conclusion, the present study indicated for the first time that prostaglandins, acting through the EP4 receptor for PGE2 mediate the bradykinin-induced sensitization of capsaicin-evoked calcium responses in rat DRG neurons. This study also illustrates that modulation of TRPV1 might occur through one or more signalling pathways including the PLC-DAG-PKC pathway and a pathway that involves arachidonic acid -DAG lipase – COX –PGE2. These results shed light on the molecular mechanism underlying the signaling pathway for bradykinin in cases of thermal allodynia and hyperalgesia and help to describe the nociceptive hypersensitivity observed in primary afferent neurons. These findings could lead to the discovery of new and more effective targets for treating pain. Therefore, blocking EP4 receptors could be a novel therapeutic avenue to prevent the development of chronic pain with fewer side effects.