Fig. 6
Strong reduction of general meningeal excitability by exogenous AEA. A Example traces of APs recorded from the peripheral part of trigeminal nerve innervating rat meninges for the control condition i.e. before any application, during application of 10 µM AEA, within the 1-min active phase of the 1st KCl pulse and within the 1-min active phase of the 2nd KCl pulse when also 10 µM AEA was present. Note the increased nociceptive firing during 10 µM AEA application that decreased during the combined application with KCl. B Time courses of spike frequency (10-s bin size) induced by two subsequent KCl pulses of 50 mM KCl and 1 µM Capsaicin in the control condition (data representation from Fig. 4B), within the combined application of 10 µM AEA with the 2nd KCl pulse, and in the presence of CB1 antagonist AM-251 (1 µM). C The ratio before and during the first 5-min of the AEA application (N = 6) was lower compared to the corresponding windows ratio in the control condition (Cntr, N = 7, data representation from Fig. 4B; Kruskal Wallis test, * = 0.03) Combined application of AEA and AM-251 counteracted the effect (N = 6, Kruskal Wallis test, * = 0.02). D The ratio of KCl-evoked APs (between the 2nd and the 1st (taken as 100%) KCl pulse) within the 1-min active phase was strongly decreased from the control (Cntr, N = 8, data representation from Fig. 4C) condition when AEA was applied (N = 6, Kruskal Wallis test, * = 0.02). Application of also AM-251 counteracted the effect (N = 6, Kruskal Wallis test, * = 0.02). E The number of APs during the 1-min active phase of 1 µM Capsaicin was reduced during the AEA application (N = 6, Kruskal Wallis test, * = 0.01) and during the combined application of AEA and AM-251 (N = 6, Kruskal Wallis test, * = 0.01) compared to the control condition (Cntr, N = 7; data representation from Fig. 4D)