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. Author manuscript; available in PMC: 2013 Nov 22.
Published in final edited form as: Biol Psychiatry. 2011 Dec 6;71(8):10.1016/j.biopsych.2011.10.032. doi: 10.1016/j.biopsych.2011.10.032

Figure 6.

Figure 6

Corticotropin-releasing factor (CRF) increases gamma-aminobutyric acid release via a protein kinase A (PKA)-dependent pathway. (A) Left panel: representative miniature inhibitory postsynaptic currents (mIPSCs) from a central nucleus of the amygdala (CeA) neuron before and during 200 nmol/mL CRF application. Right panel: a leftward shift in the cumulative frequency plot for the CeA neuron in Figure 6A indicates a shorter interevent interval during CRF application. (B) Left panel: representative mIPSCs before and during CRF application in the presence of Rp-cAMP. Right panel: cumulative frequency plot for the neuron in Figure 6C. (C) Left panel: representative mIPSCs before and during CRF application with 5 μmol/mL PKI in the internal solution. Left panel: cumulative frequency plot for the CeA neuron in Figure 6E. The leftward shift indicates a shorter interevent interval during the application of CRF with PKI. (D) Scaled average mIPSCs from the traces in Panels A, C, and E. (E) Histograms depicting the average change in mIPSC frequency (left panel) and amplitude (right panel) with CRF alone, CRF in the presence of Rp-cAMP, and CRF with PKI in the internal solution (between-subjects one-way analysis of variance: [F(2,18) = 4.409; *p < .05]).