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. 2016 Sep 7;9:80. doi: 10.3389/fnmol.2016.00080

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Copyright © 2016 Kou, Wan, Bai, Li, Hu, Zhang, Zhang, Chen, Wang, Li and Li.

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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Effects of EM2 on glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs) of neurons in spinal lamina II in the control and diabetic rats. A neuron of lamina II pictured during whole-cell patching (A). The illustrated representative traces of sEPSCs at baseline, with application of 3 μM EM2 in a neuron of lamina II from a control and a diabetic rat (B). Cumulative fraction of the inter-event interval, time decay and amplitude of sEPSCs (C) during baseline (blue) and application of EM2 (red) in the control and diabetic rats in the same neurons shown in (B). Analyses of all data in 15 neurons from six control rats and 14 neurons from 10 diabetic rats illustrated that the frequency was significantly higher in the diabetic rats (D), but there were no differences in decay time (E) and amplitude (F) between the two groups of rats. Application of EM2 decreased the frequency (D) but not the time decay (E) or the amplitude (F) of the sEPSCs. The bar chart shows that the frequency of sEPSCs was significantly reduced by EM2, but the inhibitory effects of EM2 were lower in diabetic rats (G). Mean ± SEM, *p < 0.05, **p < 0.01.