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. Author manuscript; available in PMC: 2018 Oct 1.
Published in final edited form as: Neuropharmacology. 2017 Aug 10;125:343–352. doi: 10.1016/j.neuropharm.2017.08.007

Figure 6. Neurosteroid modulation of GLIC–ρ chimeras.

Figure 6

(A) Representative agonist induced (EC20–30) currents from oocytes expressing GLIC, GABAρ, and GLIC–ρII in the absence and presence of neurosteroid isomers 5α-THDOC (upper panel) and 5β-THDOC (lower panel). Black bars represent agonist application (pH 5 for GLIC, 1µM GABA for GABAρ and pH 6 for GLIC–ρII). Open bars represent neurosteroid application, 30µM for GLIC and GLIC–ρII and 10µM for GABAρ. (B) Summary of neurosteroid modulation of EC20–30 currents from GLIC, GABAρ, GLIC–ρII and GLIC–ρIII, [(I+DRUG/I)−1]×100 (%). 5α-THDOC potentiated EC20–30 agonist mediated GABAρ currents but inhibited GLIC, GLIC–ρII and GLIC–ρIII currents. 5β-THDOC inhibited EC20–30 agonist mediated GABAρ and GLIC currents but potentiated GLIC–ρII and GLIC–ρIII currents. Data are mean±SEM from ≥ 3 oocytes.