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. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: Neuropharmacology. 2012 Dec 4;67C:337–348. doi: 10.1016/j.neuropharm.2012.11.026

Figure 4.

Figure 4

A: Representative mIPSC recordings in CeA neurons from msP, SD and Wistar rats in control condition, during application of the CRF1 antagonist R121919 (1μM) and washout. B: Mean ± SEM frequency of mIPSCs in CeA neurons from msP, SD and Wistar rats. R121919 significantly (*p< 0.05; Student’s t-test) decreased the mean mIPSC frequency in all three strains, suggesting decreased presynaptic GABA release. C: Mean ± SEM amplitude of mIPSCs in CeA neurons from msP, SD and Wistar rats. In CeA neurons from msP rats, R121919 significantly (*p< 0.05; Student’s t-test) decreased the mean mIPSC amplitude, indicating postsynaptic effects. D: Mean ± SEM frequency of mIPSCs in CeA neurons from msP rats. R121919 significantly (*p< 0.05; within-subject one-way repeated measures ANOVA) decreased the mean mIPSC frequency and blocked the ethanol-induced increase in mIPSC frequency. E: Mean ± SEM frequency of mIPSCs in CeA neurons from msP rats. R121919 significantly (*p< 0.05; within-subject one-way repeated measures ANOVA) decreased the mean mIPSC frequency and blocked the CRF-induced increase in mIPSC frequency.