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. 2017 Jun 5;149(6):661–680. doi: 10.1085/jgp.201711762

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© 2017 Amin et al.

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Figure 6. — Recovery of function in “pore-dead” constructs. (A) Example whole-cell recordings, displayed as in Fig. 3 A, for NMDARs containing double mutations in the GluN2A subunit, L812M, and a tryptophan substituted at either N816W, V820W, or S831W. Receptors containing single tryptophan substitutions of N816, V820, or S831 showed no detectable glutamate-activated whole-cell currents (Fig. 3 B and Table 1). (B) Mean current amplitudes (±SEM) at −70 mV for single or double mutation constructs. Positions that did not show detectable glutamate-activated currents are demarcated by an “X.” Number of whole-cell current recordings for each construct: GluN1/GluN2A(N816W), 9; GluN1/GluN2A(L812M/N816W), 5; GluN1/GluN2A(V820W), 8; GluN1/GluN2A(L812M/V820W), 4; GluN1/GluN2A(S831W), 9; GluN1/GluN2A(L812M/S831W), 6.