title: BDNF over-expression increases olfactory bulb granule cell dendritic spine density in vivo.
abstract: Olfactory bulb granule cells (GCs) are axon-less, inhibitory interneurons that regulate the activity of the excitatory output neurons, the mitral and tufted cells, through reciprocal dendrodendritic synapses located on GC spines. These contacts are established in the distal apical dendritic compartment, while GC basal dendrites and more proximal apical segments bear spines that receive glutamatergic inputs from the olfactory cortices. This synaptic connectivity is vital to olfactory circuit function and is remodeled during development, and in response to changes in sensory activity and lifelong GC neurogenesis. Manipulations that alter levels of the neurotrophin brain-derived neurotrophic factor (BDNF) in vivo have significant effects on dendritic spine morphology, maintenance and activity-dependent plasticity for a variety of CNS neurons, yet little is known regarding BDNF effects on bulb GC spine maturation or maintenance. Here we show that, in vivo, sustained bulbar over-expression of BDNF in transgenic mice produces a marked increase in GC spine density that includes an increase in mature spines on their apical dendrites. Morphometric analysis demonstrated that changes in spine density were most notable in the distal and proximal apical domains, indicating that multiple excitatory inputs are potentially modified by BDNF. Our results indicate that increased levels of endogenous BDNF can promote the maturation and/or maintenance of dendritic spines on GCs, suggesting a role for this factor in modulating GC functional connectivity within adult olfactory circuitry.
authors.affiliation: Department of Biomedical Science, Charles E. Schmidt College of Medicine, Florida Atlantic University, United States.
authors.forename: B
authors.initials: B
authors.lastname: McDole
authors.affiliation: Department of Biomedical Science, Charles E. Schmidt College of Medicine, Florida Atlantic University, United States.
authors.forename: C
authors.initials: C
authors.lastname: Isgor
authors.affiliation: Department of Biomedical Science, Charles E. Schmidt College of Medicine, Florida Atlantic University, United States.
authors.forename: C
authors.initials: C
authors.lastname: Pare
authors.affiliation: Department of Biomedical Science, Charles E. Schmidt College of Medicine, Florida Atlantic University, United States. Electronic address: kguthrie@health.fau.edu.
authors.forename: K
authors.initials: K
authors.lastname: Guthrie
mesh_terms: D000818:Animals; D015153:Blotting, Western; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics / Q000378:metabolism*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000235:genetics; D049229:Dendritic Spines / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D017403:In Situ Hybridization; D008297:Male; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009830:Olfactory Bulb / Q000166:cytology / Q000254:growth & development / Q000502:physiology*; D010784:Photomicrography; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D012333:RNA, Messenger; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2
keywords: GABAergic neurons; TrkB; brain-derived neurotrophic factor; dendrite morphology; dendrodendritic; spine maintenance