Figure 5.
Glucocorticoid-induced facilitation of GABA release is mediated by nitric oxide. A, The Dex (1 μm)-induced increase in amplitude (Amp) of eIPSCs was blocked by previous bath application of the NOS inhibitor l-NAME (50 μm). Traces are averages of 7–9 consecutive eIPSCs during the 3 min before l-NAME application (Control), during the last 3 min of a 10 min application of l-NAME, and during the last 3 min of a subsequent 10 min application of Dex and l-NAME. l-NAME had no effect by itself, but abolished the Dex-induced increase in eIPSC amplitude. B, Summary histogram of mean evoked IPSC amplitudes in Dex, l-NAME, and Dex + l-NAME (n = 8). C, Recording of mIPSCs 2 min before l-NAME application (Control) and following 10 min in l-NAME and 8 min in Dex (1 μm) + l-NAME. GABA currents are outward. D, Normalized running average of mean mIPSC frequency (Freq) response to Dex and l-NAME. Dexamethasone (1 μm) had no effect on mIPSC frequency in the presence of l-NAME (50 μm). E, Summary histogram of mean mIPSC frequency response to Dex in the presence of NOS antagonists. l-NAME and the nNOS-selective inhibitor NPLA (1 μm) were without effect on basal mIPSC frequency, but abolished the Dex-induced increase in mIPSC frequency. F, Summary histogram of mean mIPSC frequency response to Dex in the absence and presence of NO precursor l-arginine (L-arg, 500 μm). l-Arginine and Dex had similar, nonadditive facilitatory effects on mIPSC frequency. The effects were not influenced by the order of application of the two compounds.