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. 1999 Aug 15;19(16):6844–6854. doi: 10.1523/JNEUROSCI.19-16-06844.1999

Fig. 7.

Fig. 7.

9-aminoacridine block reveals larger fraction of channels open after the peak response for NR1A/NR2B than NR1A/NR2A.A, B, Representative traces showing NR1A/NR2A (A) or NR1A/NR2B (B) mediated current evoked by 20 msec application of 1 mmglutamate (Control, thick line) or 1 mmglutamate plus 100 μm 9-AA (9-AA, thin line). Holding potential was −60 mV. The top trace in the inset is the open tip recording at the end of the experiment. C–H, Representative traces recorded from cell expressing NR1A/NR2A (C–E) or NR1A/NR2B (F–H). Current elicited by voltage switch from −100 to +60 mV 20 msec after a 500 msec application of 1 mm glutamate plus 100 μm 9-AA (C, F,Tail current, thin lines). Current evoked by 20 msec application of 1 mm glutamate at a holding potential of +60 mV (D, G, Evoked, thick lines). E and H show same currents on expanded time scale and evoked current peaks are normalized to those of tail currents. I–K, Bars represent mean ± SEM from n = 6 different cells for each subtype.J (for NR1A/NR2A) and K (for NR1A/NR2B) compare the time constant or constants of current decay for voltage-activated currents immediately after 9-AA application (filled bars) with those for glutamate-evoked currents (open bars), both obtained at holding potentials of +60 mV. **p < 0.01 by unpairedt test. Extracellular solution contained 0.2 mm calcium.