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. 2015 Jun;93:28–40. doi: 10.1016/j.neuropharm.2015.01.001

Fig. 4.

Fig. 4

α-Bgtx binds at the β–α subunit interface of GABAARs. A, Schematic of the experimental protocol. 48 hrs after transfection, HEK-293 cells expressing eGFP and α2β2γ2 were incubated in drug for 5 min at RT followed by the addition of drug +400 nM α-Bgtx-AF555 for 10 min at RT to label cell surface receptors. The cells were washed to remove the excess α-Bgtx-AF555, fixed and imaged. B, Images of cells expressing α2β2γ2, stained with α-Bgtx-AF555 in the presence of 1 mM d-Tc, 1 mM nicotine, or 1 mM carbachol. C, Mean cell surface fluorescence of α-Bgtx-AF555 bound to surface GABAARs in the presence of d-Tc, nicotine or carbachol. D, Images of cells expressing α2β2γ2, stained with α-Bgtx-AF555 in the presence of 250 μM GABA, 50 μM bicuculline, 1 mM d-Tc, 500 nM flunitrazepam or 20 μM picrotoxin. E, Mean cell surface fluorescence of α-Bgtx-AF555 bound to GABAARs in the presence of: GABA, bicuculline, d-Tc, flunitrazepam, picrotoxin. F, 5 μM GABA-activated currents and mean (±sem) inhibition caused by 5 μM Zn2+ for HEK-293 cells expressing α2β2γ2 or α2β2 receptors, 48 h post-transfection. ***P < 0.001, **P < 0.01; n = 6–7. Scale bars 5 μm.