C– D, Histograms showing total dendrite length and total branch number of WT (WT + Cre) and BDNF f/f (BDNF f/f + Cre) mice at each time point (mean ± SEM n = 25–108 for each time point 3–4 mice per point *** p < 0.001, one-way ANOVA followed by Student's t test). B, Example images of newborn neurons expressing Cre recombinase and GFP at 2 wpi, 8 wpi and 3 mpi in WT (left) and BDNF f/f mice (right). Sample confocal projection images (right) from newborn GCs (GFP +) in the hippocampus at 8 wpi. Mice were perfused at different time points as indicated. A, Schematic diagram showing the experimental procedure for labeling newborn GCs in adult mice through retrovirus-mediated gene transfection. Therefore, BDNF expressed in adult-born GCs plays a critical role in dendrite development by acting as an autocrine factor.īDNF autocrine action dendrite development.Ĭopyright © 2015 the authors 0270-6484-10$15.00/0.Įffects of BDNF deletion in adult-born GCs on dendrite development. Furthermore, increased dendrite growth of adult-born GCs caused by voluntary exercise was abolished by BDNF deletion specifically in these neurons and elevated dendrite growth due to BDNF overexpression in these neurons was prevented by reducing neuronal activity with coexpression of inward rectifier potassium channels, consistent with activity-dependent autocrine BDNF secretion. The BDNF autocrine action was also required for the development of normal density of spines and normal percentage of spines containing the postsynaptic marker PSD-95, suggesting autocrine BDNF regulation of synaptogenesis. Furthermore, selective expression of BDNF in adult-born GCs in BDNF cKO mice fully restored normal dendrite development. This effect was mainly due to the autocrine rather than paracrine action of BDNF, because deletion of BDNF only in the newborn GCs resulted in dendrite abnormality of these neurons to a similar extent as that observed in conditional knockout (cKO) mice with BDNF deleted in the entire forebrain. Using retrovirus-mediated gene transfection, we found that deletion and overexpression of BDNF in adult-born GCs resulted in the reduction and elevation of dendrite growth, respectively. In this study, we examined the function of brain-derived neurotrophic factor (BDNF), which is expressed in adult-born GCs, in regulating their dendrite morphogenesis. Dendrite development of newborn granule cells (GCs) in the dentate gyrus of adult hippocampus is critical for their incorporation into existing hippocampal circuits, but the cellular mechanisms regulating their dendrite development remains largely unclear.
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