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. 2018 Jan 10;8:304. doi: 10.1038/s41598-017-18307-9

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© The Author(s) 2017

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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Amplitude and decay time constant of miniature end-plate currents are decreased at the NMJs in rats affected by EAMG. (A) Average of 100 individual miniature end-plate currents (mEPCs) recorded at the NMJ of healthy rat (left), rat affected by EAMG (middle) and EAMG-affected rat treated by 2 nM C547 (right). (B) Mean amplitude of mEPCs recorded in EDL muscles of healthy rats and animals affected by EAMG before and after inhibition of cholinesterases by C547 (2 nM) or pyridostigmine (Pyr, 1 µМ). (C) Mean decay time constant of mEPCs recorded in healthy rats and animals affected by EAMG before and after inhibition of cholinesterases by C547 (2 nM) or pyridostigmine (Pyr, 1 µМ). Data is presented as mean ± SEM pooled from five healthy rats and five EAMG-affected rats (5–6 end-plates per animal). Asterisk (*) indicates statistically significant difference (p < 0.05). The membrane potential was held at −60 mV.