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. 2022 Dec 22;60(3):1659–1674. doi: 10.1007/s12035-022-03162-1

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — P2 receptor antagonists do not affect corticostriatal transmission or plasticity. A, D, G Neither population spikes (PS) recorded in the dorsal striatum upon cortical stimulation in mouse brain slices nor input/output curves nor B, C, E, F, H, I high-frequency stimulation (HFS)–induced long-term-potentiation (LTP) were modified in presence of: A–C the generic P2R antagonist pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS, 20 μM); D–F the preferring P2X7 receptor (P2X7R) antagonist Brilliant Blue-G (BBG, 100 nM); G–I the selective P2X4R antagonist 5-(3-bromophenyl)-1,3-dihydro-2Hbenzofuro[3,2-e]-1,4-diazepin-2-one (5-BDBD, 20 μM). Data are mean ± SEM of 5 experiments (number of different animals tested). No significant alterations of either basal synaptic transmission or LTP magnitude were observed with any of the tested drugs (Student’s t test at p < 0.05)