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Relevant bibliographies by topics / BDNF-TrkB signaling / Dissertations / Theses

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Dissertations / Theses on the topic 'BDNF-TrkB signaling'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

歐穎嫻 and Wing-han Au. "Brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinaseB (TRKB) signaling in ovarian cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557947.

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2

Au, Wing-han. "Brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TRKB) signaling in ovarian cancer." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557947.

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3

Lee, Heow Won. "Role of BDNF in Cardiac Remodeling and Dysfunction in Rats After Myocardial Infarction." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39642.

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Myocardial infarction (MI) induced heart failure (HF) is a leading cause of morbidity and mortality over the world. Regular exercise improves quality of life and decreases hospitalization and mortality of patients with HF. In animals, exercise post MI attenuates progressive cardiac remodeling and cardiac dysfunction, and decreases neuronal activity in the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM), which are key brain nuclei contributing to sympathetic hyperactivity post MI. The peripheral and central molecular mechanisms underlying these beneficial effects of exerc

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4

Simó, Ollé Anna. "Effects of neuromuscular activity coupled to BDNF/TrkB signaling on the phosphorylation of the exocytotic proteins Munc18-1 and SNAP-25 through nPKCε and cPKCβI". Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/460898.

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A la sinapsis de la unió neuromuscular (NMJ), diverses vies de senyalització coordinen les respostes pre-/postsinàptiques i les cèl·lules glials associades. La relació entre aquestes vies modula les vesícules sinàptiques que regulen la neurotransmissió. A més, la PKC fosforila diverses molècules de l'aparell exocitòtic responsable d'aquesta regulació. Munc18-1 i SNAP-25 són substrats de PKC que juguen un paper clau en la maquinària exocitòtica. A més, la PKC està modulada per l'activitat pre-/postsinàptica al múscul esquelètic. No obstant això, encara es desconeix quines isoformes de PKC regul

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5

Barra, de la Tremblaye Patricia. "A role for CRH and HPA Activation in the Regulation of Plasticity Signaling, Neuroinflammation and Emotional/Mnesic Behavior Following Global Cerebral Ischemia in Rats." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34645.

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Depression occurs in about one third of patients with stroke and cardiac arrest. Hyperactivity of the stress system is the most commonly observed neuroendocrine change in major depressive disorder (MDD), which involves elevated levels in the cerebrospinal fluid of corticotropin-releasing hormone (CRH), a key stress neurohormone. Substantial evidence suggests that normalization of the stress system may be a requirement for successful treatment of MDD through region-specific changes in the mesocorticolimbic circuitry. Thus, alteration in the stress system may underlie the emotional and functiona

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6

Marongiu, Daniele [Verfasser]. "Interplay between BDNF,TrkB signalling and GABAergic inhibition in the visual cortex of mice / Daniele Marongiu." Mainz : Universitätsbibliothek Mainz, 2013. http://d-nb.info/1042639949/34.

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7

Hurtado, Caballero Erica. "Coordinated effects of synaptic activity and muscle contraction on cpkc regulation by pdk1 and bdnf/trkb signalling. An approach towards the amyotrophic lateral sclerosis pathophysiology." Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/457136.

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El sistema neuromuscular és un complex circuit interconnectat en el qual les motoneurones presinàptiques i cèl·lules de Schwann indiquen al múscul esquelètic com créixer, diferenciar-se i funcionar. D’altra banda, el múscul proporciona senyals, incloent les neurotrofines, que regulen la supervivència i les funcions de les motoneurones. En concret, la neurotrofina BDNF regulada per activitat, a l’unir-se al TrkB, pot activar diferents vies incloent les PKCs. Per tant, és important conèixer com opera l’activitat pre- i post-sinàptica en condicions fisiològiques per controlar la funció neuromuscu

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8

Guidi, Mònica. "Micro RNA-Mediated regulation of the full-length and truncated isoforms of human neurotrophic tyrosine kinase receptor type 3 (NTRK 3)." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7114.

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Neurotrophins and their receptors are key molecules in the development of the<br/>nervous system. Neurotrophin-3 binds preferentially to its high-affinity receptor<br/>NTRK3, which exists in two major isoforms in humans, the full-length kinaseactive<br/>form (150 kDa) and a truncated non-catalytic form (50 kDa). The two<br/>variants show different 3'UTR regions, indicating that they might be differentially<br/>regulated at the post-transcriptional level. In this work we explore how<br/>microRNAs take part in the regulation of full-length and truncated NTRK3,<br/>demonstrating that the two isof

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9

Harward, Stephen Cannada. "BDNF-TrkB Signaling in Single-Spine Structural Plasticity." Diss., 2016. http://hdl.handle.net/10161/12096.

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<p>Multiple lines of evidence reveal that activation of the tropomyosin related kinase B (TrkB) receptor is a critical molecular mechanism underlying status epilepticus (SE) induced epilepsy development. However, the cellular consequences of such signaling remain unknown. To this point, localization of SE-induced TrkB activation to CA1 apical dendritic spines provides an anatomic clue pointing to Schaffer collateral-CA1 synaptic plasticity as one potential cellular consequence of TrkB activation. Here, we combine two-photon glutamate uncaging with two photon fluorescence lifetime imaging mi

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10

Shih-Ying and 吳詩盈. "BDNF-TrkB signaling inhibits microglial activation: countering effect of aging and exercise." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/4r59hk.

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博士<br>國立成功大學<br>基礎醫學研究所<br>104<br>Aging, inflammation, and reduced brain-derived neurotrophic factor (BDNF) are associated with dopaminergic neuron loss in the substantia nigra. However, the causal relationships are unclear. We found age-related dopaminergic neuron loss lower in mice with inhibited microglial activation. BDNF and BDNF-receptor TrkB levels were positively correlated with the number of dopaminergic neurons and negatively with the degree of microglial activation. Lipopolysaccharide-induced microglial activation was attenuated by BDNF, while BDNF-induced antimicroglial activation

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11

Hokenson, Kristen Elizabeth. "BDNF signaling in epilepsy: TRKB-induced JAK/STAT pathway and phosphorylation of LSF in neurons." Thesis, 2016. https://hdl.handle.net/2144/16740.

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Epilepsy is a neurological disorder that causes recurrent and unprovoked seizures due to imbalances in synaptic transmission in distinct regions of the brain. In both human patients and animal models of epilepsy, there is a marked increase in brain-derived neurotrophic factor (BDNF), a critical signaling molecule in the brain that contributes to two divergent pathways important to disease pathology: 1) the regulation of type A receptors for the major inhibitory neurotransmitter GABA (GABAARs), and 2) aberrant neurogenesis with ectopic expression of new neurons from progenitor cells that disrup

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12

Chih-WeiChen and 陳致維. "Testectomy Acts through BDNF-TrkB Downstream Signaling Molecules PI3K and MAPK to Enhance Long-Term Potentiation in the Rat Lateral Amygdala." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/96757510381600989549.

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13

Han-TsungChi та 紀瀚雄. "Treadmill Exercise Acts through BDNF-TrkB Downstream Signaling Molecules PLCγ and PKC to Facilitate Long-Term Potentiation in the Rat Hippocampus Dentate Gyrus". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/253k6q.

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碩士<br>國立成功大學<br>生理學研究所<br>102<br>Many studies have indicated that chronic exercise training enhances learning and memory as well as long-term potentiation (LTP), the best-described neurobiological substrate of learning and memory to date. Previous studies have shown that treadmill exercise enhances passive avoidance (PA) memory by down-regulating the serotonin type 1A (5-HT1A) receptor system and up-regulating levels of brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) in the rodent hippocampus and amygdala, brain areas highly associated with PA memo

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14

Wei-JuLee та 李維儒. "17β-Estradiol Acts through BDNF-TrkB Downstream Signaling Molecules PLCγ, PKC, PI3K and MAPK to Enhance Long-Term Potentiation in the Lateral Amygdala of Ovariectomized Rats". Thesis, 2016. http://ndltd.ncl.edu.tw/handle/cq58ha.

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碩士<br>國立成功大學<br>生理學研究所<br>104<br>Long-term potentiation (LTP) is a phenomenon in which brief high-frequency stimulation (HFS) of a synaptic pathway results in long-term enhancement of the efficacy of connections made by that pathway. LTP in the lateral nucleus of amygdala (LA) has been shown to be intimately involved in the cellular changes that underlie fear memory formation. Previous studies from our laboratory have demonstrated that LA-LTP is significantly greater in female rats than in male rats. In addition, the female sex steroid 17β-estradiol(E2) mediates female’s enhanced LA-LTP. Recen

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15

Boukhatem, Imane. "La signalisation du Brain-Derived Neurotrophic Factor et ses récepteurs dans les plaquettes." Thesis, 2019. http://hdl.handle.net/1866/23992.

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Initialement découvert au cerveau, le Brain-derived neutrophic factor (BDNF) est un facteur de croissance dont les mécanismes de relâche et la signalisation ont été bien étudiés dans le système nerveux central. Il est aussi retrouvé en concentrations importantes dans la circulation où il est emmagasiné dans les plaquettes avec des niveaux pouvant atteindre 100 à 1000 fois ceux des neurones. Malgré l’abondance du BDNF dans les plaquettes, sa fonction dans la physiologie plaquettaire n’a jamais été étudiée. Le but de ce projet était donc d’investiguer le rôle du BDNF dans la fonction plaquettair

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