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. Author manuscript; available in PMC: 2009 Dec 1.
Published in final edited form as: Neuropsychopharmacology. 2009 Feb 4;34(7):1829–1842. doi: 10.1038/npp.2009.5

Figure 5. Activation of adenylyl cyclase potentiates GABAA IPSCs and occludes further potentiation by HFS.

Figure 5

(a) Single experiment showing occlusion of the HFS-induced potentiation with forskolin (10μM)-induced potentiation. Inset: Averaged GABAA IPSCs recorded during a single experiment before (black), after 20 minutes in forskolin (red) and 20 minutes after HFS (green). Calibration: 10 ms, 100 pA.

(b) Forskolin activated adenylyl cyclase to increase GABAergic transmission, while dideoxyforskolin had no effect on GABAA–mediated responses (forskolin cells, filled circles: 191 ± 22% of pre-drug values, n=10; dideoxyforskolin cells, open circles: 98 ± 6% of pre-drug values, n=3). Inset: Forskolin-induced potentiation was accompanied by a decrease in the paired pulse ratio (PPR), suggesting an increase in presynaptic GABA release after forskolin. Five-minute blocks of data are shown (PPR before forskolin: 1.02±0.13; in forskolin: 0.78±0.05; p<0.05).

(c) After the IPSCs in forskolin reached a stable potentiated level, HFS was delivered. Forskolin-induced potentiation occluded further potentiation of IPSCs by HFS (85 ± 0.6% of pre-HFS values, n=7). Only the portion of the experiment after forskolin-potentiation has plateaued is shown.