a prominent molecular mechanism of inflammatory pain, we asked if cAMP would modulate the activity of sEHIs. In these experiments normal animals that did not have an underlying painful state were tested. Remarkably prevention of the degradation of cAMP by a potent phosphodiesterase inhibitor, rolipram, allowed the sEHI to become analgesic in normal animals while the sEHIs on their own do not change nociceptive thresholds in normal animals [60]. Thus, simulation of a painful state by elevating cAMP which occurs upon the algogen PGE2 binding the prostaglandin (EP) receptors [62] activated the ability of EFAs to suppress pain related behavior.
