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. 2010 Dec 16;3:117. doi: 10.3389/fnmol.2010.00117

Figure 4.

Figure 4

(A) Mean agonist-induced current amplitudes of the construct GluA1-(TMDC)GluN1(M793Y) in absence and presence of γ2. (B) Potentiation of glutamate-evoked currents by TCM, a desensitization inhibitor. (C) Potentiation of glutamate-induced currents by γ2. Levels of significance were calculated by unpaired, two-tailed t-tests. (D) Membrane expression of point mutants of the GluN1 chimera. All mutants are expressed and integrated into the plasma membrane at higher levels than the initial chimera GluA1-(TMDC)GluN1. (E) Exemplary current traces of GluA1 wild type and GluA1-(TMDC)GluN1(M793Y). Glutamate-induced currents are shown in the top row, glutamate-induced currents in presence of TCM are shown in the top row, and kainate-evoked currents in the bottom row; currents recorded in the absence of the TARP γ2 are shown in the left half of the figure, currents observed in its presence in the right half. Please note different scaling and units.