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Molecular mechanisms of neurotrophin signaling on dendrite development and dynamics are only partly understood. To address the role of brain-derived neurotrophic factor (BDNF) in the morphogenesis of GABAergic neurons of the main olfactory bulb, we analyzed mice lacking BDNF, mice carrying neurotrophin-3 (NT3) in the place of BDNF, and TrkB signaling mutant mice with a receptor that can activate phospholipase Cgamma (PLCgamma) but is unable to recruit the adaptors Shc/Frs2. BDNF deletion yielded a compressed olfactory bulb with a significant loss of parvalbumin (PV) immunoreactivity in GABAergic interneurons of the external plexiform layer. Dendrite development of PV-positive interneurons was selectively attenuated by BDNF since other Ca2+ -binding protein-containing neuron populations appeared unaffected. The deficit in PV-positive neurons could be rescued by the NT3/NT3 alleles. The degree of PV immunoreactivity was dependent on BDNF and TrkB recruitment of the adaptor proteins Shc/Frs2. In contrast, PLCgamma signaling from the TrkB receptor was sufficient for dendrite growth in vivo and consistently, blocking PLCgamma prevented BDNF-dependent dendrite development in vitro. Collectively, our results provide genetic evidence that BDNF and TrkB signaling selectively regulate PV expression and dendrite growth in a subset of neurochemically-defined GABAergic interneurons via activation of the PLCgamma pathway.

Original publication




Journal article


J Neurobiol

Publication Date





1437 - 1451


Animals, Animals, Newborn, Blotting, Western, Brain-Derived Neurotrophic Factor, Cells, Cultured, Dendrites, Drug Interactions, Gene Expression Regulation, Developmental, Immunohistochemistry, Interneurons, Membrane Potentials, Mice, Mice, Transgenic, Nerve Tissue Proteins, Olfactory Bulb, Parvalbumins, Patch-Clamp Techniques, Phospholipase C gamma, Rats, Rats, Sprague-Dawley, Receptor, trkB, Signal Transduction, Silver Staining