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. 2016 May 12;3(3):ENEURO.0048-16.2016. doi: 10.1523/ENEURO.0048-16.2016

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Copyright © 2016 Chen et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 3. — Pharmacological blockade of MAGL or glutamate transporter enabled the spread of SSE. A, Intracellular dialysis of BAPTA (20 mm) and GDP-βS (2 mm) abolished SSE in wild-type control slices (n = 9; ***p < 0.001). The panel was taken from Figure 2A for the purpose of comparison. B, Bath application of MAGL inhibitor JZL184 (0.3 µm) substantially extended SSE (n = 7–9; ***p < 0.001), and intracellular dialysis of BAPTA and GDP-βS attenuated SSE (n = 7–8; ***p < 0.001), and the remaining SSE was abolished by the CB₁ receptor antagonist AM251 (2 µm; n = 8–9, ***p < 0.001). C, Bath application of glutamate transporter inhibitor TBOA (100 µm) extended SSE (n = 8–9; ***p < 0.001), and intracellular dialysis of BAPTA and GDP-βS did not significantly alter SSE (n = 8–9; ***p < 0.001). D, Summary of changes in EPSC amplitude under experimental conditions shown in A–C(n = 7–9; ***p < 0.001, n.s. p > 0.05).