essentially reduces all cytochrome P450 activity, interfere with bulbospinal analgesia mediated by opioid agonists [66, 67]. The mechanism of action of these findings is still under investigation but is hypothesized to take place via P450 inhibition modulating a pathway that relates presynaptic opioid receptor activation to GABA activity [68]. The EETs do not bind to opioid receptors, though they seem to contribute to opioid mediated analgesia [65, 66]. Thus in addition to the crosstalk mediated by the EFAs that occurs between the different branches within the arachidonic acid cascade there seems to be a crosstalk among multiple analgesic pathways, with EFAs contributing to the descending analgesic pathway.
