Fig. 7: BDNFpro-induced TrkB/SorCS2 targeting.

a Schematic representation of the experimental design. Step I, deletion of p75NTR in astrocytes from tamoxifen-treated p75-flox mice precludes proBDNF transfer from neurons to astrocyte following TBS. Step II, LV-BDNFprostop transduction replaces BDNFpro in astrocytes. Step III, astrocytic BDNFpro provides final increase of TrkB/SorCS2 complexes in dendritic spines and LTP maintenance. b z-stack reconstruction showing NeuN/PLATrkB/SorCS2 colocalization signal in TBS-slices from p75-flox mice transduced with LV-GFPstop or LV-BDNFprostop. Scale bars: 40 μm. The insets show the field of analysis. Scale bars: 15 μm. NeuN/PLATrkB/SorCS2 colocalization was quantified using Mander’s overlap. **p < 0.01 (unpaired t-test) (n = 4 slices, 3 mice for each experimental condition). c Dot plot shows quantification of pTrkB/TrkB colocalization in baseline- and TBS-slices from p75-flox mice transduced with LV-GFPstop or LV-BDNFprostop and control littermates using Mander’s overlap. ***p < 0.001 (unpaired t-test) (n = 4 slices, 3 mice for p75-flox mice/LV-GFPstop/TBS; n = 4 slices, 3 mice for p75-flox mice/LV-GFPstop/baseline; n = 6 slices, 4 mice for p75-flox mice/LV-BDNFprostop/TBS; n = 5 slices, 4 mice for p75-flox mice/LV-BDNFprostop/baseline; n = 5 slices, 3 mice for control littermates/TBS; n = 6 slices, 3 mice for control littermates/baseline). Data are normalized to baseline and presented as mean ± SEM.