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. 2001 Jan 15;21(2):392–400. doi: 10.1523/JNEUROSCI.21-02-00392.2001

Fig. 4.

Fig. 4.

DTNB inhibition of NMDA-evoked currents in wild-type and mutant NR1–1a/NR2A receptors. A,NMDA-evoked currents (200 μm NMDA plus 100 μm glycine) in oocytes expressing NR1–1a/NR2A, NR1–1a(C744A, C798A)/NR2A, and NR1–1a(C79S, C308S, C744A, C798A)/NR2A(C87A, C320A) receptors. DTNB (0.5 mm) still inhibited NMDA-evoked currents in NR1–1a/NR2A and NR1–1a(C744A, C798A)/NR2A receptors, but inhibition was abolished in NR1–1a(C79S, C308S, C744A, C798A)/NR2A(C87A, C320A) receptors. B,DTNB inhibition of NMDA-evoked currents from wild-type NR1–1a/NR2A receptors and various cysteine mutant combinations expressed as a percentage of the response to NMDA alone (mean ± SEM,n = 5–16). The amplitude of inhibition was measured 30 sec after the onset of DTNB and NMDA coapplication. DTNB inhibition of NMDA-evoked currents in NR1–1a(C79S, C308S, C744A, C798A)/NR2A(C87A, C320A) receptors was significantly different from that observed in wild-type NR1–1a/NR2A or subunit combinations containing only one or two pairs of mutated cysteine residues. (*p < 0.01 and †p < 0.03, ANOVA followed by Fisher's PLSD test).