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. 2009 Aug 14;20(4):898–911. doi: 10.1093/cercor/bhp156

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© 2009 The Authors

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — Voltage-dependent amplification of EPSP_KA but not EPSP_AMPA via the activation of persistent sodium current. (A) Superimposed average evoked subthreshold EPSP_AMPA recorded at threshold holding potential (−50 mV) and at Vrest (−70 mV) in granule cells from control (left, black traces) and epileptic rats (middle, red traces, in the presence of 10 μM SYM 2081); superimposed average evoked subthreshold EPSP_KA recorded in a granule cell from an epileptic rat (right, red traces, in the presence of 100 μM GYKI 52466). (B) Scatter plot of mean amplification (ratio of EPSP area at −50 vs. −70 mV) versus membrane potential. Note that EPSP_AMPA are not amplified with depolarization (left graph), both in control (black triangles, n = 5 cells) and in epileptic rats (red triangles, n = 5 cells); on the contrary, EPSP_KA in epileptic rat (right graph) are significantly amplified with depolarization (filled circles, n = 8 cells). This amplification is completely prevented by phenytoin (100–200 μM, open circles, n = 5 cells). (C) Superimposed evoked EPSP_KA recorded in the presence of phenytoin (200 μM) in epileptic rat at −50 and −70 mV. Note that the voltage-dependent amplification is completely abolished when persistent sodium current is blocked by phenytoin. (D) Superimposed evoked EPSP_KA recorded in the presence of low concentration of TTX (10 nM) in epileptic rat at −50 and −70 mV. Note that the voltage-dependent amplification is completely abolished when persistent sodium current is blocked by TTX. Trace inset shows that 10 nM TTX does not prevent neuronal firing and increases spike timing reliability. (E) Bar graph of the mean amplification (ratio of EPSP area at −50 vs. −70 mV) for EPSP_AMPA in control (n = 11 cells), EPSP_AMPA in SYM 2081 in epileptic rats (n = 5 cells), EPSP_KA in GYKI 52466 in epileptic rats (n = 13 cells, **P < 0.01), EPSP_KA in the presence of phenytoin in epileptic rats (n = 5 cells), and EPSP_KA in the presence of 10 nM TTX in epileptic rats (n = 6 cells). (F) Bar graph of EPSP-spike latency SD for EPSP_AMPA in control (n = 20 cells), EPSP_AMPA in SYM 2081 in epileptic rats (n = 5 cells), EPSP_KA in GYKI 52466 in epileptic rats (n = 17 cells, **P < 0.01), and EPSP_KA in the presence of 10 nM TTX in epileptic rats (n = 7 cells, *P < 0.05).