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. Author manuscript; available in PMC: 2012 May 1.
Published in final edited form as: Neurobiol Aging. 2009 Jun 21;32(5):821–833. doi: 10.1016/j.neurobiolaging.2009.05.012

Figure 1.

Figure 1

TrkB axonal processing is impaired in Tg2576 neurons. (A) Depicted is a schematic of the microfluidic chamber used to facilitate the study of axonal TrkB processing in CNS neurons. The neurons are plated within the somal compartment and axons grow through the microgrooves and into the axonal compartment. A volume difference between the somal and axonal compartment (40 μl) was used to generate a fluidic resistance within the microgrooves, isolating BDNF treatment to just axons. (B) Levels of Tau-1 are not altered in Tg2576 neurons when compared to wild-type (WT) neurons. β-actin served as a loading control. (C) Representative images showing TrkB (green) and Tau-1 (red) levels in axons after axonal BDNF treatment (2h). Tau-1, an axonal marker was used to normalize the TrkB labeling found in each microgroove since the number of axons that projected through each varied. (D) Quantitation of TrkB within axons following BDNF axonal treatment in wild-type neurons, in Tg2576 neurons and in Tg2576 neurons pre-treated with γ-secretase inhibitors. The data are presented as mean± SEM. * denotes p<0.0001.