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. 2024 May 7;27(6):109920. doi: 10.1016/j.isci.2024.109920

Figure 1.

Figure 1

CB1 receptor activation reduces spontaneous excitatory inputs onto A17 and AII amacrine cells

(A) Representative image of A17 amacrine cell (AC) filled with Alexa Fluor 488 (left), representative traces of sEPSCs (VHold = −60 mV) during baseline (BL) and after the bath application of WIN (1 μM, middle), and summary graphs (right) showing that WIN decreased the frequency but not the amplitude of sEPSCs recorded in A17 ACs (n = 14 cells/11 animals).

(B) Representative image (left), representative traces (middle), and summary graphs showing that WIN also decreased the frequency of sEPSCs recorded in AII ACs (n = 11 cells/8 animals). Note that a small, reduction in the amplitude was also observed.

(C) Representative traces (left) and summary graphs (right) showing that WIN-mediated effects on sEPSC frequency and amplitude in AII ACs were blocked by pretreatment with the CB1R inverse agonist AM251 (4 μM, n = 6 cells/4 animals).

(D) Pretreatment with the CB2R inverse agonist AM630 (3 μM, n = 8 cells/5 animals) did not prevent the WIN-mediated effects on sEPSC frequency and amplitude in AII ACs. Data are presented as mean ± S.E.M and open circles represent a single cell. ∗p < 0.05, ∗∗p < 0.01. Comparisons were made using paired t-tests or Wilcoxon signed-rank tests. For statistics, see Table S1.