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. 2017 Dec 4;6:e24192. doi: 10.7554/eLife.24192

Figure 2. Shisa7 effects on AMPAR desensitization rate and recovery from desensitization.

(a) Peak-scaled example trace of whole-cell recordings from HEK293 cells expressing a homomeric GluA1-containing AMPAR channel in the absence (black) or presence (blue) of Shisa7. Currents were evoked by direct application of 1 mM glutamate during 1 s. (b) Bar graphs (mean ±SEM) summarize changes in rise time (t45 = 0.091; p=0.928), desensitization time constant (t25.38 = 2.922; p=0.007) and steady-state AMPAR-mediated currents (t41 = 2.638; p=0.012). (c) Example trace of repeated 1 ms glutamate application from HEK293 cells expressing a homomeric GluA1-containing AMPAR channel in the absence (black) or presence (blue) of Shisa7. (d) Recovery of desensitization (two 1 ms glutamate application with inter-pulse interval of 20, 50, 100, 200, 300, 400, 500, 750, and 1000 ms) from HEK293 cells expressing a homomeric AMPAR channel in the absence (black) or presence (blue) of Shisa7. Inset shows a significant increase in τrecovery in the presence of Shisa7(t23.35 = −3.022; p=0.006).

Figure 2.

Figure 2—figure supplement 1. Shisa7 does not alter AMPAR kinetics in vitro or alter membrane properties in vivo.

Figure 2—figure supplement 1.

(a) Peak-scaled example traces of whole-cell recording from HEK293 cells expressing homomeric GluA1-containing AMPAR channels in the absence (black) or presence (blue) of Shisa7. Currents were evoked by direct application of 1 mM glutamate during 1 ms. (b) Bar graphs (mean ±SEM) summarize changes in rise time (p=0.593), and deactivation time (p=0.561) of AMPAR currents mediated by heteromeric AMPARs in HEK293 cells in the presence and absence of Shisa7. (c) IV-curve of homomeric GluA1-containing AMPARs expressed in HEK293 cells in the presence and absence of Shisa7 shows that Shisa7 does not alter rectification of GluA2-lacking AMPARs.