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. Author manuscript; available in PMC: 2010 Jan 1.
Published in final edited form as: Neuropharmacology. 2008 Jul 12;56(1):198–207. doi: 10.1016/j.neuropharm.2008.07.004

Figure 3.

Figure 3

Modulation of GABA currents after 4 h hypoxia. (A) Enhancement of 3 μM GABA currents by increasing concentrations of diazepam (DZ) in control cells (filled squares, n=10), 0 h (open circles, n=8), 24 h (open triangles, n=8) and 48 h (open diamonds, n=8) after 4 h hypoxia, normalized to control current amplitude. A significant increase in maximal enhancement was observed at 0 h after hypoxia (ρ<0.01) compared to control, with no change in EC50. (B) Enhancement of 3 μM GABA currents by zolpidem (ZOL) in control cells (filled squares, n=10), 0 h (open circles, n=8), 24 h (open triangles, n=6) and 48 h (open diamonds, n=8) after 4 h hypoxia. The EC50 for enhancement was unchanged, but maximal enhancement was significantly increased at the 48 h recovery time point after hypoxia (ρ<0.05). (C) Enhancement of 3 μM GABA currents by pentobarbital (PB) in control cells (filled squares, n=6), 0 h (open circles, n=2), 24 h (open triangles, n=6) and 48 h (open diamonds, n=6) after 4 h hypoxia. Maximal enhancement and EC50 were not significantly different (ρ>0.05). (D) Inhibition of 10 μM GABA currents by increasing concentrations of Zn2+ in control cells (filled squares, n=6), 0 h (open circles, n=5), 24 h (open triangles, n=6) and 48 h (open diamonds, n=6) after 4 h hypoxia. No difference in Zn2+ inhibition were observed (ρ>0.05). (See Table 4, 5)