1,2- dioleoyl- sn- glycero- 3- phosphoethanolamine- N- arachidonoyl

01/01/2018 - "While 20:4-NAPE treatment inhibited the excitatory synaptic transmission in both naive and inflammatory conditions, peripheral inflammation altered the underlying mechanisms. "
01/01/2023 - "Our results show that 20:4-NAPE application has a significant modulatory effect on spinal cord nociceptive signaling that is mediated by both TRPV1 and CB1 presynaptic receptors, whereas peripheral inflammation changes the underlying mechanism. "
01/01/2018 - "Our data indicate that 20:4-NAPE application induced mainly CB1 receptor-mediated inhibitory effects in naive animals while TRPV1-mediated mechanisms were also involved after inflammation. "
01/01/2023 - "The switch between TRPV1 and CB1 receptor activation by the AEA precursor 20:4-NAPE during inflammation may play an important role in nociceptive processing, hence the development of pathological pain."
01/01/2018 - "After inflammation, 20:4-NAPE increased sEPSCs frequency in the presence of PF514273 and this increase was blocked by SB366791. "

01/01/2023 - "The switch between TRPV1 and CB1 receptor activation by the AEA precursor 20:4-NAPE during inflammation may play an important role in nociceptive processing, hence the development of pathological pain."