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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Neuropharmacology. 2016 Nov 27;114:123–134. doi: 10.1016/j.neuropharm.2016.11.021

Figure 2. Ethanol acutely reduced the amplitude of BLA-evoked compound glutamatergic EPSPs in the medial CeA, particularly in males.

Figure 2

A,B. Representative evoked glutamatergic-EPSPs (eEPSPs) in CeM, at baseline (Control) and during 44 mM ethanol (EtOH) superfusion onto slices obtained from male (A) and diestrus female (B) rats. C. Time course of treatment effects, with ethanol application following an 8-min baseline. Inset shows quantification of the peak ethanol-induced change in eEPSP over a 4-minute bin beginning not less than 6 min into ethanol application in males vs. all females. Data are depicted as mean ± standard error percent change in eEPSP relative to control. D. Quantification of ethanol’s effect on I/O responses to 3 intermediate intensity stimuli in males vs. all females. Data are depicted as mean ± standard error percent change in eEPSP after ethanol application, normalized to control. E. Time course of treatment effects by estrous cycle, with ethanol superfusion ollowing an 8-min baseline. Estrous cycle affects ethanol’s modulation of peak eEPSP amplitude. Histograms depict mean ± standard error percent changes in peak ethanol effect relative to control. F. Estrous cycle impacts CeM neurons’ stimulus responsiveness, as measured by the I/O relationship at 3 intermediate intensity stimuli. Data are depicted as mean ± standard error percent change in eEPSP relative to control. n’s = 3–22, as listed on each panel of the graph; cells becoming unstable after drug wash-on were excluded from I/O analyses. *p<0.05 relative to control (one-sample t-test).