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. 2007 Aug 10;148(1-5):7–21. doi: 10.1016/j.neuroscience.2007.06.002

Fig. 4.

Fig. 4

The depression of eEPSC amplitude by ACPT-1 is not mediated by PKA. (A) sEPSCs recorded before and during application of forskolin (FSK, 20 μM) showing a clear increase in frequency. (B) This is confirmed by the cumulative probability analysis for pooled sEPSCs from seven neurones. (C) Averaged eEPSC responses (n=10) from the same cell as in A, showing that FSK increases eEPSC amplitude, and this is clearly shown by the pooled amplitude data in the bar chart, from the same seven neurones as in B. (D) Individual eEPSCs recorded in the presence of the specific AC inhibitor SQ22536 (50 μM) alone, and with the subsequent addition of ACPT-1 (20 μM). The agonist induced a similar depression of the eEPSC amplitude to that seen without the AC inhibitor. (E) sEPSCs recorded from the same neurone as in D showing the lack of effect of ACPT-1 on spontaneous release during inhibition of AC. (F) The bar graph summarizes changes in eEPSC amplitude with ACPT-1 during application of SQ22536 in seven neurones. (G) The cumulative probability plot shows pooled data for IEI in the same seven neurones as in F. Scale bars=10 pA, 60 ms (A); 60 pA, 20 ms (C, D); 20 pA, 20 ms (E).