Thesis (Ph. D.)--Case Western Reserve University, 2006. / [School of Medicine] Department of Neurosciences. Includes bibliographical references. Available online via OhioLINK's ETD Center.

Thesis (Ph. D.)--University of Virginia, 2001. / Spine title: Cell death in olfactory development. Includes bibliographical references (leaves 124-151). Also available online through Digital Dissertations.

Tsim Ting Yuk. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 119-135). / Abstracts in English and Chinese. / ABSTRACT --- p.i / 摘要 --- p.iii / 英漢譯名對照 --- p.v / ABBREVIATIONS --- p.vi / ACKNOWLEDGMENTS --- p.viii / Chapter 1. --- Introduction / Chapter 1.1. --- Olfactory system --- p.1 / Chapter 1.1.1. --- Olfactory bulb (OB) --- p.1 / Chapter 1.1.2. --- Accessory olfactory bulb (AOB) --- p.3 / Chapter 1.2. --- Stem cells --- p.5 / Chapter 1.3. --- Sexual differentiation --- p.8 / Chapter 1.3.1. --- Sexual dimorphic olfactory system --- p.8 / Chapter 1.3.2. --- Androgen receptor (AR) & estrogen receptor beta (ERβ) --- p.13 / Chapter 1.3.3. --- Aromatase --- p.15 / Chapter 1.3.4. --- Oligomycin sensitivity-conferringrotein (OSCP) --- p.18 / Chapter 1.4. --- rogrammed cell death (PCD) --- p.18 / Chapter 1.4.1. --- CD in the olfactory development --- p.18 / Chapter 1.4.2. --- Caspase 3 --- p.22 / Chapter 1.4.3. --- B cell leukemia/ Lymphoma 2 (Bcl-2) --- p.23 / Chapter 1.5. --- Axon guidance molecules --- p.25 / Chapter 1.5.1. --- Growth cone --- p.25 / Chapter 1.5.2. --- Mechanisms of growth cone advance --- p.26 / Chapter 1.5.3. --- Semaphorins --- p.28 / Chapter 1.5.4. --- Neuropilin --- p.31 / Chapter 1.5.5. --- lexin --- p.32 / Chapter 1.5.6. --- Collapsin response mediatorroteins (CRMPs) --- p.32 / Chapter 1.6. --- Olfactory markerroteins --- p.33 / Chapter 1.6.1. --- Markerroteins in ORNs --- p.33 / Chapter 1.6.2. --- Growth associatedrotein (GAP-43) --- p.34 / Chapter 1.6.3. --- Is the expression of GAP-43 in rat OB sexually dimorphic? --- p.36 / Chapter 1.6.4. --- Olfactory markerrotein (OMP) --- p.38 / Chapter 1.6.5. --- Golf --- p.39 / Chapter 1.7. --- Miscellaneous genes --- p.40 / Chapter 1.7.1. --- Substance (SP) --- p.40 / Chapter 1.7.2. --- Gonadotropin releasing hormone (GnRH) --- p.41 / Chapter 1.7.3. --- Metabotropic glutamate receptor 2 (mGluR2) --- p.42 / Chapter 1.7.4. --- Insulin-like growth factor binding protein-2 (IGFBP2) --- p.43 / Chapter 2. --- Materials and methods / Chapter 2.1. --- Animal study --- p.46 / Chapter 2.2. --- RNA extraction --- p.46 / Chapter 2.3. --- Quantitation of total RNA --- p.49 / Chapter 2.4. --- Reverse Transcription (RT) --- p.50 / Chapter 2.5. --- olymerase Chain Reaction (PCR) --- p.51 / Chapter 2.6. --- urification ofCRroducts --- p.55 / Chapter 2.7. --- Confirmation ofCRroducts --- p.56 / Chapter 2.8. --- Quantitation of cDNA --- p.57 / Chapter 2.9. --- Radioactive labeledCR --- p.58 / Chapter 2.10. --- Electrophoresis ofCRroducts --- p.59 / Chapter 2.11. --- Statistical analysis --- p.60 / Chapter 3. --- Results / Chapter 3.1. --- Standard curve construction --- p.61 / Chapter 3.2. --- β-actin --- p.62 / Chapter 3.3. --- Sexual differentiation related genes --- p.64 / Chapter 3.3.1. --- AR --- p.64 / Chapter 3.3.2. --- ERβ --- p.65 / Chapter 3.3.3. --- Aromatase --- p.65 / Chapter 3.3.4. --- OSCP --- p.66 / Chapter 3.4. --- CD related genes --- p.66 / Chapter 3.4.1. --- Bcl-2α --- p.66 / Chapter 3.4.2. --- Caspase 3 --- p.67 / Chapter 3.5. --- Axon guidance molecules and related genes --- p.67 / Chapter 3.5.1. --- SemaIII --- p.67 / Chapter 3.5.2. --- Neuropilin-1 --- p.68 / Chapter 3.5.3. --- lexin-1 --- p.68 / Chapter 3.5.4. --- CRMP-1 --- p.69 / Chapter 3.5.5. --- CRMP-2 --- p.70 / Chapter 3.5.6. --- CRMP-3 --- p.70 / Chapter 3.5.7. --- CRMP-4 --- p.71 / Chapter 3.6. --- Olfactory markerrotein genes --- p.71 / Chapter 3.6.1. --- GAP-43 --- p.71 / Chapter 3.6.2. --- OMP --- p.72 / Chapter 3.6.3. --- Golf --- p.72 / Chapter 3.7. --- Miscellaneous genes --- p.73 / Chapter 3.7.1. --- SubstanceP --- p.73 / Chapter 3.7.2. --- GnRH --- p.73 / Chapter 3.7.3. --- mGluR2 --- p.74 / Chapter 3.7.4. --- IGFBP-2 --- p.74 / Chapter 3.8. --- Graphs and tables --- p.75 / Chapter 4. --- Discussion / Chapter 4.1. --- Quantitation of cDNA and normalization of CR results --- p.97 / Chapter 4.2. --- Sexual differentiation related genes --- p.98 / Chapter 4.3. --- CD related genes --- p.100 / Chapter 4.4. --- Axon guidance molecule and related genes --- p.103 / Chapter 4.5. --- Olfactory markerrotein genes --- p.109 / Chapter 4.6. --- Miscellaneous genes --- p.112 / Chapter 5. --- References --- p.119

Thesis (Ph. D.)--University of Washington, 1997. / Vita. Includes bibliographical references (leaves [90]-110).

Olfactory Granule cells (GCs) are a population of inhibitory interneurons responsible for maintaining normal olfactory bulb (OB) function and circuitry. Through dendrodendritic synapses with the OBs projection neurons, the GCs regulate information sent to the olfactory cortices. Throughout adulthood, GCs continue to integrate into the OB and contribute to olfactory circuitry. However, only ~50% will integrate and survive longterm. Factors aiding in the survival and morphological development of these neurons are still being explored. The neurotrophin brain-derived neurotrophic factor (BDNF) aids in the survival and dendritic spine maturation/maintenance in several populations of CNS neurons. Investigators show that increasing BDNF in the adult-rodent SVZ stimulates proliferation and increases numbers of new OB GCs. However, attempts to replicate these experiments failed to find that BDNF affects proliferation or survival of adult-born granule cells (abGCs). BDNFs regulation of dendritic spines in the CNS is well characterized. In the OB, absence of BDNF’s receptor on abGCs hinders normal spine development and demonstrates a role for BDNF /TrkB signaling in abGCs development. In this study, we use transgenic mice over-expressing endogenous BDNF in the OB (TgBDNF) to determine how sustained increased in BDNF affect the morphology of olfactory GCs and the survival and development of abGCs. Using protein assays, we discovered that TgBDNF mice have higher BDNF protein levels in their OB. We employed a Golgi-cox staining technique to show that increased BDNF expression leads to an increase in dendritic spines, mainly the mature, headed-type spine on OB GCs. With cell birth-dating using 5-bromo-2’- deoxyuridine (BrdU), immunofluorescent cell markers, TUNEL staining and confocal microscopy, we demonstrate that over-expression of BDNF in the OB does not increase survival of abGCs or reduce cell death in the GC population. Using virally labeled abGCs, we concluded that abGCs in TgBDNF mice had similar integration patterns compared to wild-type (WT) mice, but maintained increases in apical headed-type spine density from 12 to 60 days PI. The evidence combined demonstrates that although increased BDNF does not promote cell survival, BDNF modifies GC morphology and abGC development through its regulation of dendritic spine development, maturation and maintenance in vivo. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2018. / FAU Electronic Theses and Dissertations Collection

Diss. (sammanfattning) Uppsala : Univ., 2004. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 4 uppsatser.

Thesis (Ph.D. in Neuroscience) -- University of Colorado Denver, 2007. / Typescript. Includes bibliographical references (leaves 124-137). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

Thesis (Ph.D. in Neuroscience) -- University of Colorado Denver, 2008. / Typescript. Includes bibliographical references (leaves 140-153). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

京都大学 / 新制・論文博士 / 博士(医学) / 乙第13525号 / 論医博第2271号 / 新制||医||1062(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 井上 治久, 教授 大森 孝一, 教授 古川 壽亮 / 学位規則第4条第2項該当 / Doctor of Medical Science / Kyoto University / DFAM