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. 2009 Jan 14;29(2):393–401. doi: 10.1523/JNEUROSCI.4546-08.2009

Figure 3.

Figure 3.

Distinct G-protein subunit dependence of glucocorticoid regulation of GABA synaptic inputs. A, Normalized running average of mIPSC frequency (Freq). The increase in mIPSC frequency elicited by Dex (1 μm) using a control pipette solution (n = 6) was abolished when the intracellular pipette solution contained a Gβ antibody (n = 6), but was unaffected by intracellular application of a Gαs antibody (n = 7). B, Summary histogram of the effect of Dex on mean mIPSC frequency in the presence of G-protein subunit antagonists, agonist and a PKA inhibitor. The Dex-induced increase in mIPSC frequency was not blocked by the Gαs antibody, but was abolished by the Gβ antibody. The selective Gβ-binding protein, mSIRK (0.5 μm), mimicked and occluded the Dex effect on mIPSC frequency, and the inactive mSIRK isomer, mSIRK(L94) (0.5 μm), had no effect on basal mIPSC frequency or on the Dex facilitation of mIPSC frequency. The PKA inhibitor cAMPS-Rp (50 μm) had no effect on the Dex-induced increase in mIPSC frequency. C, Summary histogram of the effect of Dex on mean mEPSC frequency in the presence of G-protein subunit antibodies and a PKA inhibitor. The Dex-induced decrease in mEPSC frequency was not affected by intracellular application of the Gβ antibody, but was abolished by the Gαs antibody and PKA inhibitor cAMPS-Rp.