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.