Skip to main content
. 2019 Jul 17;10:804. doi: 10.3389/fphar.2019.00804

Figure 4.

Figure 4

Chronic fluoxetine treatment modifies the postsynaptic response in the auditory cortex of rats. Different parameters of the fEPSPs were measured after stimulation in layer I and recording in layer II–III: (A) Representative recordings in slices from vehicle or fluoxetine-treated animals (left) followed by the NMDA-mediated response (in the presence of CNQX to block AMPA receptors) (middle) and of the GluN2A-mediated response (in the presence of CNQX + ifenprodil to block AMPA and GluN2B-containing receptors) (right). (B) Peak fEPSPs, (C) rise time (or the time at which the 67% of the peak potential is achieved), (D) total postsynaptic potential (area under the curve), and (E) percentage of blockade of the total fEPSP by CNQX (NMDA component) or by CNQX + ifenprodil (GluN2A component). Slices were perfused with Mg-free aCSF (control recording) or with aCSF in the presence of CNQX and then in the presence of CNQX + ifenprodil. For each condition, at least 32 slices were recorded, obtained from 16 animals (n = 8 control and n = 8 fluoxetine). Figures show the mean ± SEM. One way-ANOVA followed by post hoc Bonferroni test was used. *p ≤ 0.05; **p < 0.01 relative to the control within each drug condition (i.e., within each pair of red vs. white bar). For indicated comparisons among groups, unpaired t-tests were used # p ≤ 0.05; ## p < 0.01, ### p < 0.001 relative to the first bar (aCSF-control without drug addition).