Fig. 5: Chronic treatment with fluoxetine enhances PV plasticity in the hippocampus.

a–e Image analysis on PV and PNN expression in the dorsal hippocampus of control and fluoxetine-treated wild-type and PV-TrkB hCKO mice. a Representative image of PV and PNN staining. Immunostaining with PV and PNN followed by intensity analysis on PV and PNN. SP stratum pyramidale, SO stratum oriens, SR stratum radiatum. Scale bar, 50 µm. b Intensity analysis of PV expression in PV interneurons. The ratio of high and intermediate-high PV was lower after fluoxetine treatment in wild-type mice, but this difference was not observed in PV-TrkB hCKO mice. c Fluoxetine-treated wild-type mice have significantly lower percentages of PV interneurons also expressing PNNs, but this effect is blunted in PV-TrkB hCKO mice (two-way ANOVA, Treatment, F (1, 36) = 1.757, P = 0.1934; Genotype, F (1, 36) = 1.203, P = 0.2801; Fisher’s LSD post hoc test, control vs Flx: wild-type, P = 0.0138; CKO, P = 0.7571). d, e PNN intensity analysis in cells separated by PV-intensity. Fluoxetine treatment reduces PNN intensities in high (intermediate-high and high) PV-expressing cells only in WT mice (two-way ANOVA, the interaction between PV intensity and Treatment, F (1, 208) = 4.785, P = 0.0298; PV intensity, F (1, 208) = 16.92, P < 0.0001; Treatment, F (1, 208) = 3.103, P = 0.0796; Fisher’s LSD post hoc test, control vs Flx: Low, P = 0.6365; High, P = 0.0281), but not in PV-TrkB hCKO mice (two-way ANOVA, interaction, F (1, 108) = 1.326, P = 0.2520; PV intensity, F (1, 108) = 28.88, P < 0.0001; Treatment, F (1, 108) = 2.564, P = 0.1122; Fisher’s LSD post hoc test, control vs Flx: Low, P = 0.6722; High, P = 0.1075). WT, control, low, number of cells (n) = 88; WT, Flx, low, n = 79; WT, control, high, n = 28; WT, control, high,17; CKO, control, low, n = 32; CKO, Flx, low, n = 48; CKO, control, high, n = 12; CKO, control, high, 20. Bars indicate mean + SEM. *P < 0.05.