EC504-a | Popen4-b | τ-Deactivate4-c | Open Times4-d | τ-Desensitize | τ-Recovery | SS/Peak Ratio4-e | |
---|---|---|---|---|---|---|---|
μM | ms | ms | ms | ms | |||
GluR1flip | 500 | 0.4–1.0 | 0.8–1.1 | 2.5–4.1 | 147 | 0.014 | |
GluR1flop | 0.8–1.1 | 3.2–3.7 | 147 | 0.007 | |||
GluR3flip | 4.8 | 15–364-f | 0.024 | ||||
GluR3flop | 1.4 | ||||||
GluR4flip | 560 | 0.6 | 0.14, 3.3 | 3.6 | 6–144-f | 0.006, 0.040 | |
GluR4flop | 0.6 | 0.9 | 31–434-f | 0.003 | |||
GluR1flip/GluR24-g | 3.4–5.1 | 28–674-f | 0.009 | ||||
GluR1flop/GluR24-g | 2.8–8.1 | 0.004 | |||||
GluR3flip/GluR24-g | 2.9–4.9 | 15–26 | 0.015–0.022 | ||||
GluR4flip/GluR24-g | 0.5, 1.3 | 3.7–6.1 | |||||
GluR4flop/GluR24-g | 0.8–1.1 | ||||||
GluR5Q | 630 | 0.3, 0.6 | 4.1–9, 68.6 | 50, 5000 | 0.01 | ||
GluR6Q | 500 | 0.5–1.0 | 2.5 | 0.6, 2.3 | 4.3–4.9 | 1900–2400 | 0.04–0.009 |
GluR7a | 5900 | 8.4–94-h | 0.04 | ||||
GluR5Q/KA2 | 0.3 | 1.4 | 3000 | ||||
GluR6Q/KA2 | 0.4, 2.1 | 2.3 | |||||
GluR7a/KA1 | 7.6 | 0.03 | |||||
GluR7a/KA2 | 5.3 | 0.03 | |||||
NR1-1a/NR2A | 1.8 | 0.36 | 33–70, 247–3504-i | 0.06, 1.0, 3.6 | 649–750 | 300–618, 1200 | 0.28 |
NR1-1a/NR2B | 0.9 | 71, 538 | 0.6, 2, 8 | 1014 | |||
NR1-1a/NR2C | 1.0 | 260–3764-j | 0.6 | ||||
NR1-1a/NR2D | 0.4 | 0.04 | 45, 4408 | 0.10, 0.9, 2.6 | NA | NA | NA |
NA, not applicable; NR1/NR2D receptors show no apparent desensitization in the continued presence of agonist. AMPA receptor data from Lomeli et al. (1994), Mosbacher et al. (1994), Partin et al. (1996), Swanson et al. (1997b), Wahl et al. (1997), and Banke and Traynelis, (1998). Kainate receptor data from Sommer et al. (1992),Heckmann et al. (1996), Swanson et al. (1996, 1997a), Schiffer et al. (1997a), and Traynelis and Wahl (1997). NMDA receptor data from Ikeda et al. (1992), Monyer et al. (1992), Stern et al. (1992), Ishii et al. (1993), Varney et al. (1996), Krupp et al. (1998), Vicini et al. (1998), Villarroel et al. (1998), and Wyllie et al. (1998).
↵4-a EC50 values were determined for the peak response to rapid application of glutamate.
↵4-b Popen was determined for AMPA and kainate receptors using non-stationary variance analysis and depends on the phosphorylation state, with phosphatases like calcineurin favoring low Popen and kinases such as PKA favoring high Popen (Traynelis and Wahl, 1997;Banke and Traynelis, 1998). NMDA receptor Popen was determined from individual activations of single channels (Wyllie et al., 1998).
↵4-c Deactivation time constants were measured in excised membrane patches in response to a 1-ms pulse of agonist.
↵4-d Individual open times are shown even for receptors for which single activations clearly occur in bursts (e.g., NMDA receptors).
↵4-e The ratio of the steady state to peak current was determined during prolonged application of glutamate. Editing of R to G at the R/G site increases the steady-state current for GluR4flop.
↵4-f See Lomeli et al. (1994) for control of the recovery from desensitization to 1-ms pulses by editing at the R/G site.
↵4-g See Mosbacher et al. (1994) for control of desensitization kinetics by GluR2 flip and flop.
↵4-h GluR7a and GluR7b possessed similar desensitization time courses.
↵4-i Similar decay times were found with NR1 splice variants.
↵4-j Deactivation was measured from the relaxation current following rapid removal of glutamate and glycine.