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. 2002 Dec 1;22(23):10182–10191. doi: 10.1523/JNEUROSCI.22-23-10182.2002

Fig. 3.

Fig. 3.

The effects of CCh on DSI and eIPSCs are reduced by AM251 and in CB1R−/− mice. A, Representative traces from three cells in rat slices treated with the CB1R antagonist AM251 (4 μm). One DSI trial per condition is shown. DSI was abolished by AM251, and CCh (1–25 μm) did not produce notable DSI. eIPSC amplitude was not changed by 1 μm CCh (a) but was reduced by 5 μm (b) or 25 μm CCh (c). Calibration: 200 pA, 30 sec.B, Representative traces of a cell from a CB1R−/− mouse. One DSI trial per condition is shown. DSI is absent in the presence or absence of CCh. eIPSCs were reduced by 5–25 μm CCh. Calibration: 200 pA, 30 sec.C, DSI was not changed significantly by 1–25 μm CCh in the presence of 4 μm AM251 (open bars) or in CB1R−/− mice (filled bars). In AM251 data,n = 5 for 1 or 25 μm CCh, andn = 4 for 5 μm CCh. For each concentration of CCh in AM251 data, p > 0.1 (paired t tests). In CB1R−/− data,n = 4, and p > 0.1 (repeated measures ANOVA). D, eIPSC amplitude was not changed by 1 μm CCh in rat slices with AM251 (open bar;p > 0.1; paired t test) or in slices from CB1R−/− mice (filled bar; p > 0.1; paired t test after repeated measures ANOVA). The effects of 5 μm CCh on eIPSC amplitude were variable from cell to cell and were not significant (p > 0.1; same tests as 1 μm). eIPSC was significantly reduced by 25 μm CCh (p < 0.05; same tests as 1 μm).