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. 2013 Apr 18;288(23):16937–16948. doi: 10.1074/jbc.M113.463711

FIGURE 6.

FIGURE 6.

Transduction of UCH-L1 rescued Aβ-mediated retrograde transport deficits. To assess whether increasing UCH-L1 could rescue Aβ-mediated transport deficits, we measured the extent of BDNF-GFP trafficking in neurons transduced with UCH-L1. A and B, representative images demonstrate that somal levels of BDNF-GFP are increased in neurons following BDNF-GFP treatment. GFP immunoreactivity was normalized to the nuclear marker, TOTO-3. C, pretreatment with Aβ led to decrease in BDNF-GFP when compared with vehicle-treated neurons. D, the addition of UCH-L1 alone led to increased somal BDNF-GFP immunoreactivity. E, UCH-L1 rescues the deficit in BDNF-GFP trafficking caused by Aβ. F, quantification of somal BDNF levels normalized to cell number (TOTO-3-positive nuclei) reveals that Aβ causes a 60.3 ± 7.1% (*, p = 0.003) decrease in the retrograde transport of BDNF-GFP back to soma compared with vehicle-treated neurons. In the presence of UCH-L1, BDNF-GFP levels were 92.6 ± 12.0% of vehicle plus BDNF. Importantly, UCH-L1 rescued the deficit in BDNF-GFP trafficking caused by Aβ. BDNF-GFP levels were 86.3 ± 14.1% of vehicle treated and revealed that UCH-L1 restored trafficking deficits caused by Aβ oligomers (*, p = 0.04). Scale bar, 200 μm. Veh, vehicle.