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Dissertations / Theses on the topic 'Brain-derived neurotropic factor'

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Published: 10 December 2022

Last updated: 29 January 2023

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1

Khundakar, Ahmad Adam. "The effect of antidepressant treatment on brain-derived neurotropic factor expression in the rat hippocampus." Thesis, De Montfort University, 2004. http://hdl.handle.net/2086/13266.

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2

Agerman, Karin. "Specificity of neurotrophins in the nervous system : a genetic approach to determine receptor engagement by neurotrophins /." Stockholm, 2003. http://diss.kib.ki.se/2004/91-7349-730-4/.

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3

Linnarsson, Sten. "Neurotrophic factors and neuronal plasticity /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4618-3/.

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4

Gunther, Erik Christian. "Molecular mechanisms of brain derived neurotrophic factor secretion and action /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/5086.

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5

Martinez, Humberto Jose. "Nerve growth factor actions on the brain /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=744572291&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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6

Wu, Linyan, and wu0071@flinders edu au. "BRAIN DERIVED NEUROTROPHIC FACTOR TRANSPORT AND PHYSIOLOGICAL SIGNIFICANCE." Flinders University. Medicine, 2007. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20071204.113001.

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Neurotrophins are important signaling molecules in neuronal survival and differentiation. The precursor forms of neurotrophins (proneurotrophins) are the dominant form of gene products in animals, which are cleaved to generate prodomain and mature neurotrophins, and are sorted to constitutive or regulated secretory pathway and released. Brain-derived neurotrophic factor (BDNF) plays a pivotal role in the brain development and in the pathogenesis of neurological diseases. In Huntingtons disease, the defective transport of BDNF in cortical and striatal neurons and the highly expressed polyQ mutant huntingtin (Htt) result in the degeneration of striatal neurons. The underlying mechanism of BDNF transport and release is remains to be investigated. Current studies were conducted to identify the mechanisms of how BDNF is transported in axons post Golgi trafficking. By using affinity purification and 2D-DIGE assay, we show Huntingtin-associated protein 1 (HAP1) interacts with the prodomain and mature BDNF. The GST pull-down assays have addressed that HAP1 directly binds to the prodomain but not to mature BDNF and this binding is decreased by PolyQ Htt. HAP1 immunoprecipitation shows that less proBDNF is associated with HAP1 in the brain homogenate of Huntingtons disease compared to the control. Co-transfections of HAP1 and BDNF plasmids in PC12 cells show HAP1 is colocalized with proBDNF and the prodomain, but not mature BDNF. ProBDNF was accumulated in the proximal and distal segments of crushed sciatic nerve in wild type mice but not in HAP1-/- mice. The activity-dependent release of the prodomain of BDNF is abolished in HAP1-/- mice. We conclude that HAP1 is the cargo-carrying molecule for proBDNF-containing vesicles and plays an essential role in the transport and release of BDNF in neuronal cells. 20-30% of people have a valine to methionine mutation at codon 66 (Val66Met) in the prodomain BDNF, which results in the retardation of transport and release of BDNF, but the mechanism is not known. Here, GST-pull down assays demonstrate that HAP1 binds Val66Met prodomain with less efficiency than the wild type and PolyQ Htt further reduced the binding, but the PC12 cells colocalization rate is almost the same between wt prodomain/HAP1 and Val66Met prodomain/HAP1, suggesting that the mutation in the prodomain may reduce the release by impairing the cargo-carrying efficiency of HAP1, but the mutation does not disrupt the sorting process. Recent studies have shown that proneurotrophins bind p75NTR and sortilin with high affinity, and trigger apoptosis of neurons in vitro. Here, we show that proBDNF plays a role in the death of axotomized sensory neurons. ProBDNF, p75NTR and sortilin are highly expressed in DRG neurons. The recombinant proBDNF induces the dose-dependent death of PC12 cells and the death activity is completely abolished in the presence of antibodies against the prodomain of BDNF. The exogenous proBDNF enhances the death of axotomized sensory neurons and the antibodies to the prodomain or exogenous sortilin-extracellular domain-Fc fusion molecule reduces the death of axotomized sensory neurons. We conclude that proBDNF induces the death of sensory neurons in neonatal rats and the suppression of endogenous proBDNF rescued the death of axotomized sensory neurons.

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7

Palm, Kaia. "Regulation of neuronal gene expression /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980612palm.

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8

Androutsellis-Theotokis, Andreas. "The release and distribution of brain derived neurotrophic factor in brain." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266203.

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9

Kawamoto, Yasuhiro. "Immunohistochemical localization of brain-derived neurotrophic factor in adult rat brain." Kyoto University, 1997. http://hdl.handle.net/2433/202181.

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10

Roeding, Ross L., Marla K. Perna, Elizabeth D. Cummins, Daniel J. Peterson, Matthew I. Palmatier, and Russell W. Brown. "Sex Differences in Adolescent Methylphenidate Sensitization: Effects on Glial Cell-Derived Neurotrophic Factor and Brain-Derived Neurotrophic Factor." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/952.

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This study analyzed sex differences in methylphenidate (MPH) sensitization and corresponding changes in glial cell-derived neurotrophic factor (GDNF) and brain-derived neurotprhic factor protein (BDNF) in adolescent male and female rats. After habituation to a locomotor arena, animals were sensitized to MPH (5mg/kg) or saline from postnatal day (P) 33–49, tested every second day. On P50, one group of animals were injected with saline and behavior assessed for conditioned hyperactivity. Brain tissue was harvested on P51 and analyzed for GDNF protein. A second group of animals was also sensitized to MPH from P33 to 49, and expression of behavioral sensitization was analyzed on a challenge given at P60, and BDNF protein analyzed at P61. Females demonstrated more robust sensitization to MPH than males, but only females given MPH during sensitization demonstrated conditioned hyperactivity. Interestingly, MPH resulted in a significant increase in striatal and accumbal GDNF with no sex differences revealed. Results of the challenge revealed that females sensitized and challenged with MPH demonstrated increased activity compared to all other groups. Regarding BDNF, only males given MPH demonstrated an increase in dorsal striatum, whereas MPH increased accumbal BDNF with no sex differences revealed. A hierarchical regression analysis revealed that behavioral sensitization and the conditioned hyperactivity test were reliable predictors of striatal and accumbal GDNF, whereas sensitization and activity on the challenge were reliable predictors of accumbal BDNF, but had no relationship to striatal BDNF. These data have implications for the role of MPH in addiction and dopamine system plasticity.

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11

Zhu, Shun-Wei. "Brain neurotrophin levels and mouse behavior : relationship to environmental influences /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-843-6/.

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12

Goggi, Julian Luke. "Brain-derived neurotrophic factor and modulation of synaptic output." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399537.

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13

Alqudah, Mohammad. "Characterization of the neurotrophic factor Brain-Derived Neurotrophic Factor (BDNF) in intestinal smooth muscle cells." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3095.

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Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family of secreted proteins, which include in addition to BDNF, nerve growth factor (NGF) and neurotrophin 3-6 (NT-3-6). BDNF mediates its functions by activating two cell surface receptors, pan-neurotrophin receptor (P75NTR) and tropomyosin-related kinase B (TrkB) and their downstream intracellular cascades. BDNF is best known for its role in neuronal survival, regulation of neuronal differentiation, migration and activity-dependent synaptic plasticity. However, BDNF is widely expressed in non-neuronal tissues as well. The localization and the function of BDNF in intestinal smooth muscle cells (SMCs) are not well defined. Thus, the main purpose of the present study was the identification and characterization of BDNF in intestinal SMCs. Using xviii biochemical and molecular techniques, we have demonstrated in this study that BDNF is synthesized and released in rabbit intestinal longitudinal SMCs cultures. Furthermore, gut neuropeptides, Pituitary Adenylate Cyclase Activating Peptide (PACAP) and substance P (SP) increased BDNF expression and release in SMCs cultures after 24 hrs and 48 hrs incubation. We have also shown that intracellular Ca2+ levels are essential for SP stimulation of BDNF expression and secretion. Lastly, we have demonstrated that exogenous BDNF enhanced carbachol (CCh)-induced contraction of isolated longitudinal muscle strips, and this was inhibited by preincubation with TrkB inhibitor K252a and PLC inhibitor U73122 sugesting that BDNF sensitize longitudinal SMCs to CCh by activating PLC pathway, which is normally absent in those muscle cells. These results provide new insight into the mechanisms of neurotrophin (BDNF) modulation of gut function, which may lead to new therapeutic avenues for treatment of gastrointestinal disorders, and explain some of the pathological changes associated with inflammation such as hypercontractility associated with gut infection or IBD.

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14

Chen, Hui. "Neuronal Glucocorticoid Receptor Regulation of Brain Derived Neurotrophic Factor Expression." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS242/document.

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Dans le système nerveux central (SNC), l'hippocampe est une structure majeure pour les fonctions cognitives et comportementales. Le Brain-Derived Neurotrophic Factor (BDNF), un acteur clé dans ces fonctions neuronales, est fortement exprimé dans l'hippocampe. La structure du gène Bdnf murin est complexe, comportant 8 exons non codants (I à VIII), chacun avec un promoteur spécifique (1 à 8) et un exon IX codant commun. Les glucocorticoïdes (GC) exercent des actions pleiotropes sur ces processus neuronaux en se liant et en activant le récepteur des glucocorticoïdes (GR), et le récepteur des minéralocorticoïdes (MR). Le GR est un facteur de transcription, modulant la transcription de ses gènes cibles, en se liant directement aux éléments de réponse des glucocorticoïdes ou en interagissant indirectement sur d’autres facteurs de transcription. Il a été suggéré que l'expression de Bdnf est régulée par le stress et les concentrations élevées de GC. Cependant, il reste à définir si BDNF est un gène cible du GR et quels sont les mécanismes moléculaires impliqués. Dans ce travail, nous avons démontré que les fortes concentrations de GC diminuent l'expression de l'ARNm de Bdnf via le GR dans divers modèles cellulaires neuronaux. Dans des cultures primaires de neurones hippocampiques de souris et dans les cellules BZ, les transcrits de BDNF contenant l’exon IV et VI sont reprimés par le GR. Par ailleurs les transfections transitoires démontrent que l’activité du promoteur 4 est diminuée par GR. Les expériences de mutagenèse et de ChIP ont révélé que la répression induite par le GR sur l'expression et l’activité transcriptionnelle de Bdnf implique un petit fragment de 74 bp situé dans le promoteur en amont de l'exon IV. La localisation précise de l’interaction génomique du GR et les facteurs de transcription potentiels mis en jeu restent à identifier. Ce travail a contribué à une meilleure compréhension des mécanismes impliqués dans la régulation de l’expression de Bdnf par GR. Il apporte de nouveaux éléments sur les interactions moléculaires et fonctionnelles entre la signalisation GC et celle de BDNF dans les neurones, d’importance majeure dans la physiopathologie du SNC
In the central nervous system (CNS), the hippocampus is a structure of major importance for cognitive and behavioral functions. The brain-derived neurotrophic factor (BDNF), a key player in such neuronal functions is highly expressed in the hippocampus. Rodent Bdnf gene structure is relatively complex, composed of 8 noncoding exons (I to VIII), each one with a specific promoter (1 to 8), and one common coding exon IX. Glucocorticoids (GC) exert pleiotropic actions on neuronal processes by binding to and activating the glucocorticoid receptor (GR), as well as the mineralocorticoid receptor (MR). GR functions as a transcription factor, directly by interacting to glucocorticoid response elements or indirectly by interacting with other transcription factors, leading to the regulation of target gene transcription. It has been suggested that Bdnf expression is regulated by stress and high GC concentrations. However, it remains to define whether Bdnf is a GR target gene and what are the underlying molecular mechanisms. Herein, we demonstrate that high GC levels downregulate total Bdnf mRNA expression via GR in various in vitro neuron-like cellular models. In primary cultures of mouse hippocampal neurons and BZ cells, BDNF IV- and VI-containing transcripts are involved in this regulatory mechanism. Moreover, in transient transfections, promoter 4 activity was reduced by activated GR. Furthermore, ChIP analysis and mutagenesis experiments demonstrate that the GR-induced repression on Bdnf expression and transcriptional activities occurs through GR binding to a small 74 bp promoter sequence upstream of exon IV. The exact GR binding site on DNA and its putative transcription factor partners are currently under investigation. Altogether, these findings contribute to a better understanding of the mechanisms by which GR represses BDNF expression. Our study brings new insights into the molecular interactions between GC signaling and BDNF signaling in neurons, both important pathways in the pathophysiology of the CNS

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15

Advani, Tushar M. "Brain derived neurotrophic factor deficient mouse a putative model of allostatic overload : a dissertation /." San Antonio : UTHSC, 2008. http://proquest.umi.com.libproxy.uthscsa.edu/pqdweb?did=1588771861&sid=7&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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16

Robinson, Amy Ann. "Quantification of brain-derived neurotrophic factor expression in the aging monkey brain." Thesis, Boston University, 2013. https://hdl.handle.net/2144/11035.

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Thesis (Ph.D.)--Boston University
While early studies of normal aging largely focused on the loss of neurons as a basis of cognitive aging, current studies of both aging humans and the rhesus monkey model of normal aging demonstrate that forebrain neurons are largely preserved. Instead, MRI and electron microscopic analyses show that age-related changes in the white matter are good predictors of cognitive impairment. White matter changes include an increase in damaged myelin sheaths as well as a loss of myelinated fibers. To explore potential causes of the white matter alterations, the expression of genes related to myelination and axonal survival were examined revealing age-related alterations in the expression of 9 genes in grey matter and 7 in subcortical white matter of the inferior parietal lobule (IPL). Four were selected for further analysis. Of these, brain-derived neurotrophic factor (BDNF) had a statistically significant decrease in expression in the cortical grey matter of the IPL at both the level of gene expression and of protein expression. In 27 male and female rhesus monkeys ranging from young to old, the precursor form of BDNF (proBDNF) was significantly decreased while the mature form was preserved. In order to understand the localization of the age-related decline in proBDNF, immunohistochemical reactivity was quantified in the IPL and in the hippocampus. In the IPL there was a significant decrease in total immunohistochemical reactivity. Further analysis showed that there was an increase in the number of proBDNF positive somata while there was no change in the smaller extrasomal puncta. This increase in cell bodies expressing proBDNF despite the age-related decrease in total proBDNF immunohistochemical density suggests disruption of post-translational processing and/or transport out into the processes. In contrast to the IPL, there was no change in proBDNF density in the hippocampus with age. However, in the hippocampus but not the IPL, proBDNF immunohistochemical reactivity was sexually dimorphic with higher levels in the female monkeys compared to males. While the significance of the change in proBDNF levels for myelin damage is unclear, alteration in this neurotrophin may play a role in the axon loss that accompanies myelin degradation.

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17

Klein, Inna. "Einfluss des Brain-derived neurotrophic factor auf Schizophrenie und Gedächtnisleistungen." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-162685.

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Die Schizophrenie ist eine psychiatrische Erkrankung,die phänotypisch in vielgestaltigen Querschnittsbildern auftreten kann.Die Äthiopathogenese der Schizophrenie ist bis heute nicht geklärt.Es wird aber davon ausgegangen, dass sie einem polygenen Erbgang folgt und multifaktorielle Bedingungen zum Ausbruch der Krankheit führen.Ein alternativer Ansatz versucht nun mithilfe von klar definierten Endophänotypen Gene zu identifizieren, die mit neuroanatomischen, neurophysiologischen oder biochemischen Korrelaten einer Erkrankung assoziiert sind.In Zusammenhang mit der Schizophrenie gehören Lern- und Gedächtnisfunktionen zu den häufig untersuchten Endophänotypen. Das Gen für den Brain-Derived-Neurotrophic-Factor (BDNF) auf Chromosom 11 ist ein Neurotrophin, das im adulten ZNS protektiv und regenerativ auf Neuronen und Motoneuronen wirkt. BDNF wird stark im Hippocampus exprimiert, einer Hirnregion, die in Lern- und Gedächtnisfunktionen involviert ist. Es konnte gezeigt werden, dass BDNF in die hippocampalen Funktionen der Langzeitpotenzierung eingreift. Unter Berücksichtigung der Omnipräsenz des BDNF im humanen Gehirn liegt auch die Vermutung nahe, dass veränderte Genexpression oder Funktionalität dieses Neurotrophins neuronale Krankheiten begünstigen oder bedingen können. In diesem Zusammenhang wird auch eine Assoziation von BDNF mit Schizophrenie diskutiert. Ein im humanen BDNF-Gen häufig vorkommender Polymorphismus ist der SNP rs6265 an Position 196 der mRNA. Er bewirkt einen Aminosäureaustausch von Valin nach Methionin und wurde bereits intensiv in Zusammenhang mit Schizophrenie untersucht. Die vorliegende Studie untersuchte an 135 schizophrenen Patienten kaukasischer Abstammung und 313 gesunden Kontrollprobanden deutscher Abstammung, ob ein Zusammenhang zwischen dem rs6265 und Schizophrenie oder Gedächtnisleistungen nachzuweisen ist. Mit einer adaptierten deutschen Fassung der Welcher Memory Scale Revised (WMS-R) wurde bei allen Studienteilnehmern Gedächtnisleistungen erfasst. Anschließend erfolgten die Analysen der Allel- und Genotypfrequenzen sowie die Zuordnung zu den Ergebnissen aus den Gedächtnistests. Im Ergebnis konnte in der Fall-Kontroll-Assoziationsstudie keine signifikante Assoziation zwischen dem rs6265 und Schizophrenie festgestellt werden. Darüber hinaus konnte in der Endophänotypenstudie keine Assoziation zwischen rs6265 und Gedächtnisleistungen nachgewiesen werden. Ein Trend zeigte sich aber im Untertest „Verbales Gedächtnis“ des WMS-R. Dabei erzielten Met-Homozygote im Durchschnitt bessere Leistungen als Träger des Val-Allels. Ob der rs6265 die Gedächtnisleistungen oder die Suszeptibiltät für Schizophrenie beeinflusst, konnte mit dieser Arbeit nicht abschließend geklärt werden. Folgestudien mit strikten Ein- und Ausschlusskriterien und größeren Stichproben sind nötig, um diese Frage abschließend zu klären.

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18

Balog, Brian Michael. "Brain-Derived Neurotrophic Factor Mediates Recovery from Stress Urinary Incontinence." University of Akron / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=akron1602113592326106.

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19

Wardle, Rinda A. "Modulation of inhibitory synaptic transmission by brain-derived neurotrophic factor /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3094613.

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20

Traver, Kyle Leann. "Environmental Enrichment-Mediated Neuroprotection Against Traumatic Brain Injury:Role of Brain-Derived Neurotrophic Factor." Wright State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=wright1307129480.

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21

Hing, Benjamin. "Investigating differential regulation of BDNF promoter IV activity by upstream polymorphic evolutionary conserved regions : implications for mood disorders and cognitive disfunction." Thesis, University of Aberdeen, 2011. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=185597.

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Major depressive disorder (MDD) and bipolar disorder (BD) are psychiatric diseases that affect behavior and impair cognition. A gene important to these disorders is the brain derived neurotrophic factor (BDNF) which is involved in processes controlling neuroplasticity. Previous studies have suggested that BDNF expression levels have to be finely regulated for normal mental health and cognition. This study therefore aimed to identify cis-regulatory elements that regulate BDNF promoter IV (BP4), which plays a role in mood and cognition, and investigated how polymorphisms in these cis-regulatory elements might alter BP4 activity contributing to MDD and BD. BP4-LacZ transgenic mice and primary neuron cultures were used to show that BP4 was active in the hippocampus, cortex and amygdala and responded to PKC, KCl and Wnt signaling activation. Using comparative genomics, two highly conserved regions were identified, BE5.1 and BE5.2, which contain the rs10767664 and rs12273363 polymorphisms respectively. Reporter gene assays in primary cultures derived from these brain structures showed that BE5.1 and BE5.2 were responsible for “filtering” or “gating” the effects of different combination of activated signal transduction pathways on BP4. Thus, BE5.1 increased BP4 response to forskolin in cortical cultures while abolishing BP4 response to PMA in hippocampal cultures. Similarly, BE5.2 permitted BP4 response to KCl and combined forskolin and PMA treatment, but not individual forskolin and PMA treatment nor LiCl in cortical cultures. Significantly, the minor allele of rs12273363, which has been associated with MDD and BD susceptibility, acted as a more potent repressor of BP4 response to neuron depolarization by KCl and PKA/PKC activation in different primary cultures. The possible relevance of these findings to the role of altered BDNF expression in MDD and BD are discussed.

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22

Hasche, Anja. "Bindung von ATP an die Neurotrophine NGF und BDNF als Voraussetzung für ihre neuroprotektive Wirkung." Münster Schüling, 2008. http://d-nb.info/989241386/04.

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23

Lam, Chi-tat. "Identification of brain-derived neurotrophic factor (BDNF) as a novel angiogenic factor in tumor angiogenesis." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290355.

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24

Berghuis, Paul. "Brain-derived neurotrophic factor and endocannabinoid functions i GABAergic interneuron development /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-125-8/.

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25

Von, dem Bussche Mary. "The role of brain-derived neurotrophic factor in cortical motor learning." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3284226.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed January 11, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.

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26

REIBEL, FOISSET SOPHIE. "Role du brain-derived neurotrophic factor dans l'epileptogenese chez le rat." Université Louis Pasteur (Strasbourg) (1971-2008), 1999. http://www.theses.fr/1999STR13037.

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L'epilepsie est une pathologie s'accompagnant de modifications biochimiques et morphologiques a l'origine de la recurrence des crises epileptiques, ou au contraire protegeant le cerveau de la survenue de nouveaux episodes critiques. Les neurotrophines, dont l'expression est modulee dans differents modeles d'epilepsie, pourraient participer a ces phenomenes de neuroplasticite. En particulier, une augmentation importante de l'expression du brain-derived neurotrophic factor (bdnf) est observee dans l'hippocampe. Afin d'evaluer le role de cette neurotrophine dans l'epileptogenese, l'effet de perfusions intrahippocampiques chroniques de bdnf a ete etudie dans le modele de l'embrasement de l'hippocampe chez le rat. Le bdnf ralentit l'evolution de l'embrasement, un effet qui se prolonge plusieurs jours au-dela de la periode de perfusion. A l'inverse, une perfusion d'oligonucleotides antisens bloquant la synthese de bdnf accelere la progression de l'embrasement. L'action protectrice du bdnf apparait specifique de l'hippocampe et de ce facteur neurotrophique : le nerve growth factor aggrave l'evolution de l'embrasement et le glial cell line-derived neurotrophic factor est sans effet. L'etude des mecanismes de l'effet protecteur du bdnf suggere qu'il n'est pas lie a une modification du bourgeonnement des fibres moussues du gyrus dentele, phenomene de neuroplasticite accompagnant l'embrasement. Nos resultats suggerent l'implication du neuropeptide y. En effet, ce neuropeptide diminue l'excitabilite hippocampique dans des modeles de crises epileptiques in vitro et in vivo. Cet effet semble resulter de l'activation des recepteurs y2 et/ou y5. Une perfusion chronique de neuropeptide y dans l'hippocampe ralentit l'embrasement de cette structure, et un effet aggravant est observe a la suite d'une perfusion d'anticorps anti-neuropeptide y. Enfin, l'application chronique de bdnf entraine une augmentation de l'expression de neuropeptide y dans l'hippocampe, qui suit le meme decours temporel que l'effet inhibiteur du bdnf sur l'embrasement de l'hippocampe. Ces resultats suggerent donc que le bdnf exerce un controle endogene de l'epileptogenese initiee dans l'hippocampe, et que cet effet pourrait etre secondaire a une modulation de l'expression de neuropeptide y dans cette structure.

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27

Tsuchida, Atsushi. "Action Mechanism of Brain-Derived Neurotrophic Factor in Regulating Glucose Metabolism." Kyoto University, 2002. http://hdl.handle.net/2433/149508.

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28

Ingram, James David. "The identification of inhibitors of nerve growth factor and brain-derived neurotrophic factor." Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/422241/.

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Chronic pain affects up to 43% of the UK population, with 12% reporting moderate to severely limiting chronic pain.1-2 This incidence rate rises with age, with 62% of over 75s being diagnosed.1 The current standard of care for chronic pain almost exclusively involves COX-1, COX-2 or μ-opioid receptor inhibitors and considerable research has been conducted in this area. Despite this, the current state of pharmacological treatments is seen by patients as decidedly lacking, with the prevailing opinion being one of concern for efficacy, side effects and addiction. Recent drug advances suggest a promising new area for development may be found in inhibiting neurotrophins or their receptors: both animal modelling and clinical trials show that significant reduction of pain sensation (nociception) may be found in the inhibition of these proteins. This is supported by Pfizer’s Tanezumab, which recently (June 2017) received FDA fast-track approval status for the treatment of chronic pain in patients with osteoarthritis and chronic lower back pain. This monoclonal antibody binds to nerve growth factor (βNGF) to prevent it binding to its receptor, and has been shown to dramatically reduce nociception. Despite this, Tanezumab shows room for improvement: a meta-analysis of trials involving Tanezumab for treatment of osteoarthritis of the knee revealed significant discontinuations due to adverse effects.3 A Phase III trial for osteoarthritic hip pain (while successful) also showed an increase in the required number of hip replacements for those taking the drug.4 Further development is therefore sought, and this research documents the initial hit discovery and development of a number of neurotrophin inhibitors. Initially this was sought through the development of a high throughput screening platform using a reverse two-hybrid system, however this proved unsuccessful. Phage display was therefore employed and successfully identified a number of peptides which bound to either βNGF or another promising neurotrophin target, mBDNF. This adherence was then tested for its target specificity, and an ELISA screen developed to assess agonist/antagonist activity. Peptides were then synthesised and further assays were attempted to ascertain binding data. Finally, the biological activity of the lead peptides was tested against TrkB/PC12 cells in western blot and morphology assays. In conclusion, this research identified several antagonists and antagonists of the neurotrophin-receptor interaction for βNGF and mBDNF.

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29

Zhou, Xiangdong. "Brain-derived Neurotrophic Factor in Autonomic Nervous System: Nicotinic Acetylcholine Receptor Regulation and Potential Trophic Effects." Connect to full-text via OhioLINK ETD Center, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1130160629.

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Thesis (Ph.D.)--Medical University of Ohio, 2005.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: Joseph F. Margiotta. Includes abstract. Document formatted into pages: iii, 226 p. Title from title page of PDF document. Bibliography: pages 80-92,130-139,149-225.

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30

Angelucci, Francesco. "Antidepressive and antipsychotic treatments : effects on nerve growth factor and brain-derived neurotrophic factor in rat brain /." Stockholm : Karolinska Univ. Press, 2002. http://diss.kib.ki.se/2002/91-7349-226-4.

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31

Wissman, Anne Marie. "Neurotrophins and seasonal plasticity in the avian song control system /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10661.

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32

Wang, Shiyang. "The role of TRKB receptors in regulation of coronary microvascular endothelial cell angiogenesis /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1543605071&sid=5&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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33

Montag, Christian. "Die revidierte reinforcement sensitivity theory eine experimentell-biologische Überprüfung." Hamburg Kovač, 2008. http://d-nb.info/993570275/04.

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34

Liu, Ping. "Blood brain-derived neurotrophic factor (BDNF) expression in normal humans and schizophrenic patients." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31352121.

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35

Hansson, Anita Christiane. "Gluco- and mineralocorticoid receptor regulation of regional brain neurotrophism /." Stockholm : Karolinska institutets bibl, 2002. http://diss.kib.ki.se/2002/91-7349-280-9.

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36

Berk, Benjamin-Andreas. "Brain-derived neurotrophic factor-induzierte neuroprotektive Osmoregulation der Müller-Gliazelle der Rattenretina." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-170385.

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Einleitung: Die Ausbildung eines Netzhautödems ist eine Hauptursache für die Verschlechterung des Sehvermögens bei ischämisch-hypoxischen und inflammatorischen Netzhauterkrankungen. Neben der erhöhten Permeabilität der Blut-Retina-Schranke trägt eine Wasserakkumulation in Netzhautzellen zur Ausbildung eines Netzhautödems bei. Müllerzellen regulieren die retinale Ionen- und Osmohomöostase, indem sie einen transzellulären Ionen- und Wassertransport vermitteln. Zudem kontrollieren Müllerzellen die Größe des Extrazellularraumes, indem sie bei neuronaler Aktivität eine Zellkörperschwellung – ausgelöst durch eine Verkleinerung der extrazellulären Osmolarität – verhindern. Unter pathologischen Bedingungen ist die Volumenregulation gestört, sodass Müllerzellen bei Hypoosmolarität anschwellen. Diese Müllerzellschwellung und eine Glutamat-induzierte Schwellung retinaler Neurone tragen zur Ausbildung eines zytotoxischen Netzhautödems bei. Neuroprotektive Faktoren wie BDNF (brain-derived neurotrophic factor) und bFGF (basic fibroblast growth factor) stimulieren das Überleben retinaler Neurone und verzögern so die retinale Degeneration. Zielstellung: Es war zu zu ermitteln, ob BDNF die zytotoxische Schwellung von Müller- und Bipolarzellen der Rattennetzhaut verhindert. Material und Methoden: Es wurden Netzhautschnitte und isolierte Müller- und Bipolarzellen von 55 adulten Long-Evans-Ratten (durchschnittlich 8-15 Zellen pro Versuchsreihe) verwendet. Eine osmotische Schwellung von Müller- und Bipolarzellen wurde durch eine Superfusion der Schnitte oder der Zellen mit einer 60%igen hypoosmolaren Lösung in Ab- oder Anwesenheit von Bariumchlorid induziert. Die maximale Querschnittsfläche von Müller- und Bipolarzellsomata wurde vor und nach einer vierminütigen Superfusion mit einem konfokalen Laserscanningmikroskop aufgezeichnet. Die nach der Superfusion ermittelte Querschnittsfläche wurde zu den anfänglich gemittelten Kontrollwerten in Beziehung gesetzt und prozentual als Mittelwert mit Standardfehler bestimmt. Mit Hilfe des Prism-Statistikprogramms (Graphpad) wurden die Ergebnisse mittels einem one-way ANOVA Test und einem nachfolgenden Bonferroni\'s multiple comparison Test sowie durch einen Mann-Whitney U Test statistisch analysiert. Ergebnisse: Bei Anwesenheit von BDNF wurde die osmotische Schwellung von Müllerzellen konzentrationsabhängig sowohl in Netzhautschnitten als auch in isolierten Zellen inhibiert. Ebenso inhibierte BDNF konzentrationsabhängig die Schwellung von Bipolarzellen in Netzhautschnitten, jedoch nicht in isolierten Zellen. In Schnitten von postischämischen Netzhäuten bewirkte BDNF eine Schwellungsinhibition von Müllerzellen, nicht aber von Bipolarzellen. Mit pharmakologischen Blockern wurde die durch BDNF induzierte Signalkaskade untersucht. Die BDNF-Schwellungsinhibition von Müllerzellen wurde durch eine Aktivierung von TrkB bewirkt. Die TrkB-Aktivierung führte in Müllerzellen zu einer Transaktivierung von FGF-Rezeptoren sowie zu einer Aktivierung einer glutamatergen-purinergen Signalkaskade, von der bekannt ist, dass sie die osmotische Müllerzellschwellung unterdrückt. Da bFGF die osmotische Müllerzellschwellung inhibiert, wird die Transaktivierung der FGF-Rezeptoren wahrscheinlich durch eine BDNF-induzierte Freisetzung von bFGF aus Müllerzellen vermittelt. Die Ergebnisse lassen vermuten, dass BDNF indirekt auf Bipolarzellen wirkt, indem es eine Freisetzung von Faktoren wie bFGF aus Müllerzellen induziert. Schlussfolgerungen: Die Schwellungsinhibition von Müller- und Bipolarzellen könnte ein neuroprotektiver Mechanismus von BDNF in der Netzhaut darstellen. Während BDNF direkt TrkB auf Müllerzellen aktiviert, ist die Inhibition der Bipolarzellschwellung indirekt und durch die Ausschüttung von glialen Faktoren wie bFGF vermittelt. Der Verlust des Effektes von BDNF auf die Bipolarzellschwellung in ischämischen Netzhäuten könnte darauf zurückzuführen sein, dass gliotische Müllerzellen keine glialen Faktoren mehr in Reaktion auf BDNF freisetzen. Der Verlust des glialen Einflusses auf die Bipolarzellvolumenhomöostase könnte zur Neurodegeneration in der ischämischen Netzhaut beitragen
Introduction: Tissue edema is a major blinding complication of ischemic-hypoxic and inflammatory retinal diseases. In addition to the hyperpemeability of the blood-retinal barrier, water accumulation in retinal cells resulting in cellular swelling may contribute to the development of retinal edema. Müller glial cells regulate the retinal ion and water homeostasis by allowing transcellular ion and water fluxes. During neuronal activity Müller cells control the extracellular space volume by autocrine inhibition of cellular swelling caused by the reduction of extracellular osmolarity. However, under pathological conditions, Müller cells are not capable to regulate their volume so that they swell rapidly under hypoosmolarity. The osmotic swelling of Müller glial cells and the glutamate induced swelling of retinal neurons contribute to the development of cytotoxic retinal edema. Various neuroprotective factors including brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (bFGF) stimulate the survival of retinal neurons and thus delay the retinal degeneration. Objective: The objective of the study is to determine whether BDNF inhibits the osmotic swelling of Müller and bipolar cells of the rat retina. Material and Methods: Retinal slices and freshly isolated Müller and bipolar cells of 55 adult Long-Evans rats (in average 8-15 cells per trial) were used. Osmotic swelling of Müller and bipolar cells was induced by superfusion of retinal slices or isolated cells with a 60% hypoosmotic extracellular solution in the absence or presence of barium chloride. The maximal cross-sectional area of Müller and bipolar cell somata was recorded before and after a four minute-long superfusion by using a laser scanning microscope. To determine the extent of cell soma swelling, the cross-sectional area of the cell body extent after superfusion was related to the former averaged cross-sectional area. Results were given as means with standard error as percent values. Statistical analysis was made with Prism (Graphpad) and the significance was determined by the One-way ANOVA test followed by Bonferroni\'s multiple comparison test and the Mann-Whitney U test, respectively. Results: We found that BDNF inhibits dose-depending the osmotic swelling of Müller cells in retinal slices and of isolated cells. BDNF also inhibited dose-depending the osmotic swelling of bipolar cells in retinal slices; however, it did not inhibit the osmotic swelling in isolated bipolar cells. In slices of postischemic retinas, BDNF inhibited the swelling of Müller cells but not the swelling of bipolar cells. The BDNF induced signal transduction cascade was examined by simultaneous administration of blocking agents with the receptor agonists in the hypoosmotic solution. The BDNF-induced inhibition of the osmotic Müller cell swelling was mediated by activation of TrkB. Activation of TrkB in Müller cells results in transactivation of FGF receptors and in an activation of a glutamatergic-purinergic signal transduction cascade which is known to inhibit the osmotic swelling of the cells. Since bFGF also inhibits the osmotic swelling of Müller cells, it can be assumed that the transactivation of FGF receptors is mediated by a BDNF-induced release of bFGF from Müller cells. The results suggest that the effect of BDNF on bipolar cells is indirect by inducing a subsequent release of glial factor from Müller cells such as bFGF. Conclusion: The results show that BDNF inhibits the osmotic swelling of Müller and bipolar cells. The inhibition of cytotoxic cell swelling may contribute to the neuroprotective action of BDNF in the retina. While BDNF acts directly in Müller cells, the BDNF-induced inhibition of the bipolar cell swelling is indirect and mediated by the release of glial factors such as bFGF from Müller cells. The abrogation of the BDNF-induced inhibition of the osmotic bipolar cell swelling in the postischemic retina could be explained with the impairment of the release of glial factors by Müller cells. The abrogation of the Müller cell-mediated regulation of the bipolar cell volume could contribute to the neuronal degeneration in the ischemic retina

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37

Peterson, Daniel J., Elizabeth D. Cummins, Stephen B. Griffin, and Russell W. Brown. "Methylphenidate Conditioned Place Preference: Role of D1 Receptors and Brain-derived Neurotrophic Factor." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/961.

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Methylphenidate (trade name: Ritalin) produced a more robust conditioned place male as compared to female juvenile rats. This effect was blocked by a D1 antagonist (SCH 23390), which resulted in a conditioned place aversion in male as compared to female rats. Effects on Brain-derived neurotrophic factor (BDNF) will be reported.

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38

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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39

Lam, Chi-tat, and 林知達. "Identification of brain-derived neurotrophic factor (BDNF) as a novel angiogenic factor in tumor angiogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290355.

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40

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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41

Liu, Ping, and 劉苹. "Blood brain-derived neurotrophic factor (BDNF) expression in normal humans and schizophrenic patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31352121.

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42

Lang, Susanne. "Imaging brain-derived neurotrophic factor-mediated calcium signaling and plasticity in developing neurons." Diss., [S.l.] : [s.n.], 2007. http://edoc.ub.uni-muenchen.de/archive/00006770.

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43

Pfaffenseller, Bianca, Flavio Kapczinski, Amelia L. Gallitano, and Fábio Klamt. "EGR3 Immediate Early Gene and the Brain-Derived Neurotrophic Factor in Bipolar Disorder." FRONTIERS MEDIA SA, 2018. http://hdl.handle.net/10150/627052.

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Bipolar disorder (BD) is a severe psychiatric illness with a consistent genetic influence, involving complex interactions between numerous genes and environmental factors. Immediate early genes (IEGs) are activated in the brain in response to environmental stimuli, such as stress. The potential to translate environmental stimuli into long-term changes in brain has led to increased interest in a potential role for these genes influencing risk for psychiatric disorders. Our recent finding using network-based approach has shown that the regulatory unit of early growth response gene 3 (EGR3) of IEGs family was robustly repressed in postmortem prefrontal cortex of BD patients. As a central transcription factor, EGR3 regulates an array of target genes that mediate critical neurobiological processes such as synaptic plasticity, memory and cognition. Considering that EGR3 expression is induced by brain-derived neurotrophic factor (BDNF) that has been consistently related to BD pathophysiology, we suggest a link between BDNF and EGR3 and their potential role in BD. A growing body of data from our group and others has shown that peripheral BDNF levels are reduced during mood episodes and also with illness progression. In this same vein, BDNF has been proposed as an important growth factor in the impaired cellular resilience related to BD. Taken together with the fact that EGR3 regulates the expression of the neurotrophin receptor p75NTR and may also indirectly induce BDNF expression, here we propose a feed-forward gene regulatory network involving EGR3 and BDNF and its potential role in BD.

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44

Ray, Sutapa Jones Kevin R. "Brain-derived neurotrophic factor is required for normal peripheral nerve development and regeneration." Diss., Connect to online resource, 2005. http://wwwlib.umi.com/dissertations/fullcit/3165831.

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45

Leavesley, Rachel Claire. "Expression and regulation of brain-derived neurotrophic factor in rat dorsal root ganglia." Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409124.

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46

Currie, James. "Blood concentration of brain-derived neurotrophic factor (BDNF) and physical activity in humans." Thesis, Oxford Brookes University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543844.

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47

Szabo, Ashley J. "Brain-Derived Neurotrophic Factor Genotype and Cognitive Functioning in Individuals with Cardiovascular Disease." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1278634648.

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48

Bergin, Stephen Michael. "Hypothalamic brain-derived neurotrophic factor regulates lymphocyte immunity, energy balance, and cancer progression." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487669797216355.

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49

Okano, Takayuki. "Cell-gene delivery of brain-derived neurotrophic factor to the mouse inner ear." Kyoto University, 2008. http://hdl.handle.net/2433/135804.

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Merrill, David A. "Mechanisms underlying age-related cognitive decline and sensitivity to brain-derived neurotrophic factor /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2002. http://wwwlib.umi.com/cr/ucsd/fullcit?p3059907.

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