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. 2017 Jul 27;11:226. doi: 10.3389/fncel.2017.00226

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Copyright © 2017 Koroleva, Mustafina, Yakovlev, Hermann, Giniatullin and Sitdikova.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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NaHS evokes calcium transients in TG neurons. (A) Representative traces recorded from cultured TG neurons. NaHS (100 μM) and capsaicin (Caps, 1 μM) were applied for 2 s to TG ganglion cells loaded with fluo 3-AM (5 μM). Neurons were distinguished from other cell types due to Ca²⁺ responses induced by potassium depolarization (50 mM KCl for 2 s). In neuron 1 TRPV1 inhibitor capsazepine (capz, 10 μM) abolished NaHS induced Ca²⁺ transient; in neuron 2 capsazepine did not affect NaHS induced Ca²⁺ transient; in neuron 3 TRPA1 inhibitor HC 030031 (50 μM) abolished NaHS evoked response. (B) Graph indicating populations of capsaicin and NaHS sensitive TG neurons and their overlap. In a total of 251 imaged neurons (selected by their response to KCl) 104 (41%) were activated by NaHS (100 μM) and 107 (43%) by capsaicin (1 μM). In 59% of capsaicin sensitive cells NaHS also induced an increase of intracellular Ca²⁺ (63 cells from 107, gray area). (C) Percentage of cells responding to NaHS (100%) after inhibition of TRPV1 (Capz + NaHS) and TRPA1 (HC 030031 + NaHS) receptors.