FIG. 2.

BDE-47 and BDE-49 and their hydroxylated metabolites reduce axon length in cultured hippocampal neurons. Cells dissociated from P1 rat hippocampi were exposed to vehicle or varying concentrations of BDE-47, BDE-49, 6-OH-BDE-47, or 4′-OH-BDE-49 beginning 3 h after plating. After a 48 h exposure, DIV 2 neurons were fixed and immunostained for tau-1. A, Representative photomicrographs of DIV 2 hippocampal neurons exposed to vehicle, BDE-47 (200 nM) or BDE-49 (200 nM). B, Quantification of axon length in tau-1 immunopositive cells in cultures exposed to BDE-47 or BDE-49 or (C) 6-OH-BDE-47 or 4′-OH-BDE-47. Data presented as the mean ± SE (n = 70–90 neurons from 3 independent dissections in all groups except for the 20 pM group in which n = 40 neurons from 3 independent dissections). **P < .01, ***P < .001 relative to vehicle control. Scale bar = 10 µm.