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. 2018 Jan 23;8:1431. doi: 10.1038/s41598-018-19624-3

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© The Author(s) 2018

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Pharmacological signature of ATP-dependent HTPC Ca²⁺ signals. (a–d) Representative original traces (f₃₄₀/f₃₈₀ versus time) of [Ca²⁺]_c transients recorded from individual HTPCs challenged with ATP (1000 µM (a,b); 30 µM (c,d); 5 s; arrows) under control conditions and during different biophysical/pharmacological treatments. Signals are abolished in absence of external Ca²⁺ (a), essentially unaffected by the P2RX7 receptor antagonist A438079 (10 µM (b)), and strongly or partly reduced in presence of PPADS (c) or TNP-ATP (d), respectively. Treatment duration (pre-incubation) is indicated by horizontal bars. (e) Bar chart quantifying the effects of different conditions on [Ca²⁺]_c response amplitudes (black bars). Data are means ± SEM, normalized to control conditions (i.e., prior stimulation; white bars). Numbers of cells are indicated above bars. Asterisks (*) denote statistical significance, p < 0.05 (paired t-test).