Skip to main content
. Author manuscript; available in PMC: 2016 Aug 6.
Published in final edited form as: Neuroscience. 2015 May 29;300:307–313. doi: 10.1016/j.neuroscience.2015.05.051

Figure 1. Etomidate produced similar modulation on β3-α1-δ/β3-α1 receptors expressed with different amount of cDNA transfections.

Figure 1

A, Representative whole cell current traces evoked by saturating GABA (1 mM) and co-application of saturating GABA (1 mM) and etomidate (3.2 μM) with etomidate pre-applied for β3-α1-δ/β3-α1 receptors transfected with 2.0 µg cDNAs. The solid lines indicated the application of GABA, and the dashed lines denoted the application of etomidate. The grey trace was the GABA current, whose peak current amplitude was normalized to that of the current evoked by GABA and etomidate to show the alterations of desensitization and deactivation induced by etomidate. B, The mean fold of enhancement of GABA (1 mM) currents by etomidate for β3-α1-δ/β3-α1 receptors transfected with 0.6, 2.0 and 6.0 µg cDNAs, respectively. C, The reduction of the extent of desensitization by etomidate for β3-α1-δ/β3-α1 receptors transfected with 0.6, 2.0 and 6.0 µg cDNAs, respectively. D, The increase in the weighted deactivation time constant (τw) by etomidate for β3-α1-δ/β3-α1 receptors transfected with 0.6, 2.0 and 6.0 μg cDNAs, respectively. In panel C and D, the filled bars represented the properties of currents evoked by GABA, and the open bars represented those by GABA plus etomidate. Error bars denoted S.E.M. *, Significantly different from GABA control at p < 0.05; ** p < 0.01; *** p < 0.001.