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. 2008 May 15;586(Pt 14):3425–3446. doi: 10.1113/jphysiol.2008.154609

Figure 5. Effect of extracellular Mg2+ on glutamate-induced Ca2+ influx in isolated RGCs.

Figure 5

A, fura-2 ratio trace for an RGC, in HBSS containing 0.8 mm Mg2+, exposed to 10, 100 and 1000 μm glutamate (plus 10 μm glycine). Responses to lower glutamate concentrations (≤ 100 μm) were attenuated with Mg2+ present, but note that RGC still responded to 200 μm kainate (indicating AMPA/kainate-Rs were not inhibited by the extracellular Mg2+). B and C, representative trace (B) and mean normalized Ca2+ influx (change in [Ca2+]i +1 s.d.) (C) for RGCs (n = 12) treated with 10 μm glutamate in the absence or presence of 0.8 mm Mg2+. D and E, fura-2 ratio traces illustrating effect of NMDA-R antagonist MK-801 (10 μm) (D) and AMPA/kainate-R antagonist NBQX (25 μm) (E) on RGC Ca2+ influx evoked by 1000 μm glutamate (plus 10 μm glycine) in HBSS containing 0.8 mm Mg2+. F, mean data (+1 s.d.) for effect of NMDA-R antagonists (hatched bars) and AMPA/kainate-R antagonist (filled bar) on glutamate-induced Ca2+ influx (normalized to initial response; dashed line). *P < 0.05, **P < 0.01, Friedman ANOVA, Tukey, compared to initial and recovery responses.