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. 2021 Jan 13;14:604583. doi: 10.3389/fnins.2020.604583

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Copyright © 2021 Castillo-Rolón, Ramírez-Sánchez, Arenas-López, Garduño, Hernández-González, Mihailescu and Hernández-López.

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) and the copyright owner(s) 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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Nicotine effects are mediated through α7 but not α4β2 nAChRs. (A) Current traces showing that MLA (100 nM), a selective antagonist of the α7 nAChRs, completely blocked the effects of nicotine on sEPSCs, control condition (left), 10 min after nicotine plus MLA (middle), and nicotine washout (right). (B) Normalized time-frequency histogram showing the lack of effect of nicotine in the presence of MLA (n = 6). (C) Current traces showing that DHβE (100 nM), a selective antagonist of the α4β2 nAChRs did not block the effect of nicotine on sEPSCs. (D) Normalized time-frequency histogram showing that nicotine increased the frequency of sEPSCs in the presence of DHβE (n = 6). (E) Bar graph illustrating a summary of the data (Mann–Whitney U-test). **p < 0.01, ***p < 0.001.