Figure 1
CRF enhances synaptic transmission in the CeLC in slices from normal animals. (A) Concentration-response relationship of CRF effects on monosynaptic EPSCs (numbers of neurons tested with each concentration are indicated). Peak amplitudes were averaged for each concentration of CRF and expressed as percent of predrug control (set to 100%). Concentration-response curve was obtained by non-linear regression analysis using the formula y = A + (B − A)/[1 + (10C/10X)D], where A is the bottom plateau, B top plateau, C = log(EC50), and D is the slope coefficient (GraphPad Prism software). *** P < 0.001, Bonferroni posttests compared to predrug. (B-E) Synaptic facilitation by CRF (10 nM, 12 min) was blocked by co-administration of an antagonist for CRF1 (NBI27914, NBI; 1 μM, 12 min) but not for CRF2 (astressin-2B, AStr2B; 1 μM, 12 min). (B, C) Monosynaptic EPSCs recorded in ACSF (Predrug), during CRF, and during CRF together with NBI27914 (B) or astressin-2B (C). Individual traces are the average of 8–10 EPSCs. (D) CRF increased input–output function significantly (n = 7 neurons). NBI27914 (n = 5) decreased the effect of CRF. Input–output curves were generated by plotting peak EPSC amplitude (pA) as a function of afferent fiber volley stimulus intensity (μA). (E) Astressin-2B (n = 5) had no significant (ns) effect on CRF-induced synaptic facilitation (n = 7). *,**,*** P < 0.05, 0.01, 0.001, Bonferroni posttests compared to predrug. ## P < 0.01, Bonferroni posttests compared to CRF. CeLC neurons were recorded at −60 mV in slices from naïve untreated animals. Symbols and error bars represent means ± SEM.