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. 2017 Feb 28;11:43. doi: 10.3389/fncel.2017.00043

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Copyright © 2017 Zhang, Wu, Shi, Xu, Chu, Cui and Qiu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and 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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Blockade of the cannabinoid receptor 1 (CB1) abolishes ethanol-induced inhibition of spontaneous CS activity. (A) Representative traces showing the spontaneous activities of a PC in treatments of ACSF, ethanol (300 mM) and ethanol + AM251 (5 μM). Arrows denote CSs. (B) Pooled data showing the pause in SSs in treatments of ACSF, ethanol and ethanol + AM251. (C) Summary of data showing the normalized amplitude of the AHP in treatments of ACSF, ethanol and ethanol + AM251. (D,E) Bar graphs showing the effect of ethanol on the normalized spikelet number (D) and AUC (E) of CSs in treatments of ACSF, ethanol and ethanol + AM251. Arrows indicate spontaneous CSs. n = 6 cells per group. *P < 0.05, vs. ACSF; ^#P < 0.05, vs. ethanol.