Relevant bibliographies by topics / BDNF-TrkB signaling

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Academic literature on the topic 'BDNF-TrkB signaling'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "BDNF-TrkB signaling"

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Feng, Ning, Sabine Huke, Guangshuo Zhu, et al. "Constitutive BDNF/TrkB signaling is required for normal cardiac contraction and relaxation." Proceedings of the National Academy of Sciences 112, no. 6 (2015): 1880–85. http://dx.doi.org/10.1073/pnas.1417949112.

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BDNF and its associated tropomyosin-related kinase receptor B (TrkB) nurture vessels and nerves serving the heart. However, the direct effect of BDNF/TrkB signaling on the myocardium is poorly understood. Here we report that cardiac-specific TrkB knockout mice (TrkB−/−) display impaired cardiac contraction and relaxation, showing that BDNF/TrkB signaling acts constitutively to sustain in vivo myocardial performance. BDNF enhances normal cardiomyocyte Ca2+ cycling, contractility, and relaxation via Ca2+/calmodulin-dependent protein kinase II (CaMKII). Conversely, failing myocytes, which have in
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Fu, Xiuping, Yanrui Yang, Chenchang Xu, et al. "Retrolinkin cooperates with endophilin A1 to mediate BDNF–TrkB early endocytic trafficking and signaling from early endosomes." Molecular Biology of the Cell 22, no. 19 (2011): 3684–98. http://dx.doi.org/10.1091/mbc.e11-04-0308.

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Brain-derived neurotrophic factor (BDNF) binds to its cell surface receptor TrkB to regulate differentiation, development, synaptic plasticity, and functional maintenance of neuronal cells. Binding of BDNF triggers TrkB dimerization and autophosphorylation, which provides docking sites for adaptor proteins to recruit and activate downstream signaling molecules. The molecular mechanisms underlying BDNF–TrkB endocytic trafficking crucial for spatiotemporal control of signaling pathways remain to be elucidated. Here we show that retrolinkin, a transmembrane protein, interacts with endophilin A1 a
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Spaeth, Andrea M., Scott E. Kanoski, Matthew R. Hayes, and Harvey J. Grill. "TrkB receptor signaling in the nucleus tractus solitarius mediates the food intake-suppressive effects of hindbrain BDNF and leptin." American Journal of Physiology-Endocrinology and Metabolism 302, no. 10 (2012): E1252—E1260. http://dx.doi.org/10.1152/ajpendo.00025.2012.

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Brain-derived neurotrophic factor (BDNF) and TrkB receptor signaling contribute to the central nervous system (CNS) control of energy balance. The role of hindbrain BDNF/TrkB receptor signaling in energy balance regulation is examined here. Hindbrain ventricular BDNF suppressed body weight through reductions in overall food intake and meal size and by increasing core temperature. To localize the neurons mediating the energy balance effects of hindbrain ventricle-delivered BDNF, ventricle subthreshold doses were delivered directly to medial nucleus tractus solitarius (mNTS). mNTS BDNF administr
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Taylor, Kathryn, Helena Zhang, Alexa Hui, Shawn Gillespie, and Michelle Monje. "TBIO-06. BDNF-TRKB SIGNALING REGULATES NEURON-GLIOMA SYNAPTOGENESIS AND PROMOTES TUMOR PROGRESSION." Neuro-Oncology 22, Supplement_3 (2020): iii468. http://dx.doi.org/10.1093/neuonc/noaa222.834.

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Abstract Pediatric high-grade gliomas (pHGG) are a devastating group of diseases that urgently require novel therapeutic options. We have previously demonstrated that pHGGs hijack mechanisms of brain development and plasticity to their advantage. Here, we investigated the role of microenvironmental BDNF on pediatric gliomas, independent of the NTRK fusion events commonly identified in infant HGG. Genetic deletion or pharmacological blockade of NTRK2 (TrkB), in patient-derived pediatric glioma increases survival in multiple DIPG and pGBM patient-derived orthotopic xenograft models. Unlike the p
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Fontanesi, Cecilia, Svetlana Kvint, Giuseppe Frazzitta, et al. "Intensive Rehabilitation Enhances Lymphocyte BDNF-TrkB Signaling in Patients With Parkinson’s Disease." Neurorehabilitation and Neural Repair 30, no. 5 (2015): 411–18. http://dx.doi.org/10.1177/1545968315600272.

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Background. In a combined animal and human study, we have previously found that a 5-day treatment that enhances cortical plasticity also facilitates brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling and increases activated TrkB and N-methyl-d-aspartate receptor (NMDAR) association in both the cortex and the peripheral lymphocytes. Patients with Parkinson’s disease (PD), in general, show decreased cortical plasticity, as demonstrated by electrophysiological and behavioral studies. Here, we test the hypothesis that an exercise program that improves motor functi
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Jin. "Regulation of BDNF-TrkB Signaling and Potential Therapeutic Strategies for Parkinson’s Disease." Journal of Clinical Medicine 9, no. 1 (2020): 257. http://dx.doi.org/10.3390/jcm9010257.

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Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase receptor type B (TrkB) are widely distributed in multiple regions of the human brain. Specifically, BDNF/TrkB is highly expressed and activated in the dopaminergic neurons of the substantia nigra and plays a critical role in neurophysiological processes, including neuro-protection and maturation and maintenance of neurons. The activation as well as dysfunction of the BDNF-TrkB pathway are associated with neurodegenerative diseases. The expression of BDNF/TrkB in the substantia nigra is significantly reduced in
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Kang, Seong Su, Zhentao Zhang, Xia Liu та ін. "TrkB neurotrophic activities are blocked by α-synuclein, triggering dopaminergic cell death in Parkinson’s disease". Proceedings of the National Academy of Sciences 114, № 40 (2017): 10773–78. http://dx.doi.org/10.1073/pnas.1713969114.

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BDNF/TrkB neurotrophic signaling is essential for dopaminergic neuronal survival, and the activities are reduced in the substantial nigra (SN) of Parkinson’s disease (PD). However, whether α-Syn (alpha-synuclein) aggregation, a hallmark in the remaining SN neurons in PD, accounts for the neurotrophic inhibition remains elusive. Here we show that α-Syn selectively interacts with TrkB receptors and inhibits BDNF/TrkB signaling, leading to dopaminergic neuronal death. α-Syn binds to the kinase domain on TrkB, which is negatively regulated by BDNF or Fyn tyrosine kinase. Interestingly, α-Syn repre
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Gangarossa, Giuseppe, Sylvie Perez, Yulia Dembitskaya, Ilya Prokin, Hugues Berry, and Laurent Venance. "BDNF Controls Bidirectional Endocannabinoid Plasticity at Corticostriatal Synapses." Cerebral Cortex 30, no. 1 (2019): 197–214. http://dx.doi.org/10.1093/cercor/bhz081.

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AbstractThe dorsal striatum exhibits bidirectional corticostriatal synaptic plasticity, NMDAR and endocannabinoids (eCB) mediated, necessary for the encoding of procedural learning. Therefore, characterizing factors controlling corticostriatal plasticity is of crucial importance. Brain-derived neurotrophic factor (BDNF) and its receptor, the tropomyosine receptor kinase-B (TrkB), shape striatal functions, and their dysfunction deeply affects basal ganglia. BDNF/TrkB signaling controls NMDAR plasticity in various brain structures including the striatum. However, despite cross-talk between BDNF
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McCarthy, Deirdre M., Kaly A. Mueller, Elisa N. Cannon, et al. "Prenatal Cocaine Exposure Alters BDNF-TrkB Signaling in the Embryonic and Adult Brain." Developmental Neuroscience 38, no. 5 (2016): 365–74. http://dx.doi.org/10.1159/000453609.

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Prenatal cocaine exposure remains a major public health concern because of its adverse effects on cognitive function. Although the molecular mechanisms underlying the cognitive impairment are not fully understood, brain-derived neurotrophic factor (BDNF) signaling via its receptor tyrosine kinase B (TrkB) is emerging as a potential candidate. We used a mouse model to examine the impact of ongoing cocaine exposure on BDNF expression in the dorsal forebrain on embryonic day 15 (E15) as well as the long-term effects of prenatal cocaine exposure on BDNF-TrkB signaling in the frontal cortex in earl
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Zou, Wujun, Xiaoyan Hu, and Liang Jiang. "Advances in Regulating Tumorigenicity and Metastasis of Cancer Through TrkB Signaling." Current Cancer Drug Targets 20, no. 10 (2020): 779–88. http://dx.doi.org/10.2174/1568009620999200730183631.

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The clinical pathology of various human malignancies is supported by tropomyosin receptor kinase (Trk) B TrkB which is a specific binding receptor of the brain-derived neurotrophic factor (BDNF). TrkB and TrkB fusion proteins have been observed to be over-expressed in many cancer patients. Moreover, these proteins have been observed in multiple types of cells. A few signaling pathways can be modulated by the abnormal activation of the BDNF/TrkB pathway. These signaling pathways include PI3K/Akt pathway, transactivation of EGFR, phospholipase C-gamma (PLCγ) pathway, Ras-Raf-MEK-ERK pathway, Jak
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Dissertations / Theses on the topic "BDNF-TrkB signaling"

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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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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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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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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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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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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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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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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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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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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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Book chapters on the topic "BDNF-TrkB signaling"

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Hashimoto, Kenji. "Brain-Derived Neurotrophic Factor (BDNF): TrkB Signaling in Depression – Biomarker and Novel Therapeutic Target." In Melatonin, Neuroprotective Agents and Antidepressant Therapy. Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2803-5_37.

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Vatanashevanopakorn, Chinnavuth, Amit Grover, Arup R. Nath, et al. "Studying BDNF/TrkB Signaling: Transcriptome Analysis from a Limited Number of Purified Adult or Aged Murine Brain Neurons." In Brain-Derived Neurotrophic Factor (BDNF). Springer New York, 2017. http://dx.doi.org/10.1007/7657_2017_3.

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Nath, Arup R., Roy Drissen, Fei Guo, Claus Nerlov, and Liliana Minichiello. "Studying BDNF/TrkB Signaling: High-Throughput Microfluidic Gene Expression Analysis from Rare or Limited Samples of Adult and Aged Central Neurons." In Brain-Derived Neurotrophic Factor (BDNF). Springer New York, 2017. http://dx.doi.org/10.1007/7657_2017_4.

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Korte, Martin. "BDNF and TrkB-Mediated Signalling Supports Processes of Metaplasticity and Long-Term Memory Formation." In Synaptic Tagging and Capture. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1761-7_10.

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Wong, Jenny. "Neurotrophin Signaling and Alzheimer’s Disease Neurodegeneration − Focus on BDNF/TrkB Signaling." In Trends in Cell Signaling Pathways in Neuronal Fate Decision. InTech, 2013. http://dx.doi.org/10.5772/53364.

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Frost, Douglas O. "Chapter 3 BDNF/trkB signaling in the developmental sculpting of visual connections." In Progress in Brain Research. Elsevier, 2001. http://dx.doi.org/10.1016/s0079-6123(01)34004-9.

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Kwatra, Mohit, Sahabuddin Ahmed, Samir Ranjan Panda, Vegi Ganga Modi Naidu, and Nitika Gupta. "Molecular Mechanisms, Therapeutic Targets and Pharmacological Interventions: An Update." In Background and Management of Muscular Atrophy. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95996.

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Muscles are the enriched reservoir of proteins in the body. During any workout or exercise, the demand in the form of energy is essentially required by the muscle. Energy expenditure of skeletal muscle is more dependent on the type of demand. There is particular homeostasis within the body that avoid surplus energy expenditure and this prevents any muscle loss. Muscle atrophy is termed as the loss of skeletal muscle mass due to immobility, malnutrition, medications, aging, cancer cachexia, variety of injuries or diseases that impact the musculoskeletal or nervous system. Hence, atrophy within the skeletal muscle initiates further cause fatigue, pain, muscle weakness, and disability in human subjects. Therefore, starvation and reduced muscle mass further initiate numerous signaling pathways including inflammatory, antioxidant signaling, mitochondria bio-energetic failure, AMP-activated protein kinase (AMPK), Sirtuin 1(SIRT1), BDNF/TrkB/PKC, Autophagy, ubiquitin-proteasome systems, etc. Here, in this chapter, we will mention molecular mechanisms involved in therapeutic targets and available Pharmacological Interventions with the latest updates.
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Azogu-Sepe, I., and H. Plamondon. "Stress Responsiveness of BDNF/TrkB Signaling in the Neuroendocrine System and Future Implications." In Stress: Genetics, Epigenetics and Genomics. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-813156-5.00013-3.

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S. Weeks, Benjamin, Samuel D. Weeks, Amanda Kim, Landon Kessler, and Pedro P. Perez. "Physiological and Cellular Targets of Neurotrophic Anxiolytic Phytochemicals in Food and Dietary Supplements." In Functional Foods [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97565.

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Diet impacts anxiety in two main ways. First anxiety can be caused by deficiencies in antioxidants, neurotransmitter precursors, amino acids, cations and vitamins and other cofactors. Second, anxiety can be reduced by anxiolytic nutraceuticals which are food molecules that bind to molecular targets of the amygdala and the hypothalamus-pituitary–adrenal axis (HPA-axis). Anxiety is a feeling of fear that arises from a perceived threat and can be a beneficial coping mechanism to threats and stressors. However excessive anxiety is a disorder that interferes with healthy responses to stressors. The amygdala is responsible for assigning value to a threat or stressor and triggering the HPA-axis to support the body wide system responses to the threat. The amygdala also communicates with the neuroplastic learning and memory centers of the hippocampus to fix or set a learned value to the threat. Interestingly, many anxiolytic nutraceuticals that show benefits in human clinical trials have neurotrophic activity and increase neuronal plasticity. Moreover, anxiolytic nutraceuticals either act like the neurotrophins, nerve growth factor (NGF), brain derived neurotrophic factor (BDNF and neurotrophin-3 (NT3) by either directly binding to or potentiating the tyrosine receptor kinase (TRK) family of receptors (TRKA, TRKB and TRKC) and activating the ERK1/2 signal transduction pathway associated with neurite outgrowth and neural plasticity. This chapter will explore the neuritogenic activity of clinically proven plant-based anxiolytic nutraceuticals and examine the commonality of TRKA-C receptors and the ERK1/2 signaling pathway in the pharmacological and nutraceutical treatment of anxiety disorders.
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Conference papers on the topic "BDNF-TrkB signaling"

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Dragunas, Guilherme, Manon Woest, Susan Nijboer, et al. "BDNF-TrkB signaling mediates cholinergic neuroplasticity in asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa4957.

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