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. 2020 Sep;27(9):380–389. doi: 10.1101/lm.050666.119

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© 2020 Fontaine et al.; Published by Cold Spring Harbor Laboratory Press

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Figure 5. — mGluR-LTD is also dependent on CB1R. (A) LTD was measured as the average percentage of change in the fEPSP slope relative to baseline for minutes 55–60 as a result of the wash of the group I mGluR agonist DHPG (30 µM, indicated as black bar). Dashed bar represents the duration of exposure of pharmacological inhibitors. (B,D) Establishment of mGluR-LTD (−21.96% ± 3.68%, n = 8 slices) does not occlude further synaptic depression by 900 × 1 Hz LFS (−41.86 ± 4.97%, n = 8 slices P = 0.00506) (C) DHPG leads to long-term depression of the fEPSP (−21.96 ± 3.68%, n = 8 slices) and pharmacological inhibition of mGluR₅ significantly attenuated this LTD (−10.18 ± 3.50%, n = 9 slices, P = 0.035) while CB1R inhibition of blocked the LTD maintenance (−0.44 ± 3.20%, n = 5 slices, P = 0.001). Dots represent the average amounts of LTD for each slice that make up the average (indicated as the bar) for each group. Error bars throughout represent the standard error of the mean. Statistical significance was achieved by a two-tailed t-test compared against control and P < 0.05 is indicated by a *.