Fig. 7
AEA analgesia and its interaction with TRPV1 receptors. A Time courses of spike frequency (10-s bin size) induced by APs recorded from the peripheral part of trigeminal nerve innervating rat meninges within the 1-min active phase of the 2nd KCl pulse in combination with 10 µM AEA or with the co-application of 10 µM AEA and 20 µM capsazepine. Note the non-significant changes in nociceptive firing during applications of 10 µM AEA and the combination of 10 µM AEA and 20 µM capsazepine. Notably, capsaicin-induced firing decreased during the combined application of 10 µM AEA and 20 µM capsazepine. B No difference was observed between the APs ratio before and during 10 min capsazepine comparing to the Aps ratio of the same tine windows in the control condition. C The ratio of APs (before/during application of exogenous AEA, N = 5) for the 5-min baseline returned to the control baseline level in presence of capsazepine (N = 6, Mann Whitney U test, ** = 0.004). D The percentage between the number of APs induced by the 1st and 2nd KCl pulse for the 1-min within AEA was not affected by the application of both 10 µM AEA and 20 µM capsazepine. E The number of APs during the 1-min active phase of 1 µM Capsaicin when also AEA was applied (N=5) was reduced after application of both 10 µM AEA and 20 µM capsazepine (N = 6, Mann Whitney U test, ** = 0.008)