Figure 4

Inhibition of PKA, but not PKC, blocks CRF-induced synaptic facilitation. (A) Original recordings of monosynaptic EPSCs (average of 8–10 traces). Facilitatory effects of CRF (10 nM) were blocked by co-administration of a PKA inhibitor (KT5720, 1 μM). (B) Summary of time course data for the sample of CeLC neurons (n = 5). Peak amplitudes of EPSCs recorded during drug application were expressed as percent of predrug control values (set to 100%). Symbols and error bars represent means ± SEM. *,** P < 0.05, 0.01, compared to predrug before CRF; ^## P < 0.01, compared to the data point immediately before KT5720 application; ANOVA with Bonferroni posttests. (C) Time course data for prolonged application of CRF without a PKA inhibitor (n = 6). Display as in (B). *** P < 0.001, compared to predrug, Dunnett’s multiple comparison tests. (D) Individual traces (average of 8–10) of monosynaptic EPSCs show that the facilitatory effect of CRF (10 nM) was not blocked by co-administration of a PKC inhibitor (GF109203x, 1 μM). (E) Time course data for GF109203x effects (n = 5). Significant facilitation by CRF persisted during coapplication of GF109203x. Display as in (B). *** P < 0.001, compared to predrug, Dunnett’s multiple comparison tests. Statistical analysis was performed on raw data.