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Journal articles on the topic 'BDNF-TrkB signaling'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

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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2

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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3

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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6

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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7

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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8

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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9

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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10

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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11

Suzuki, Shingo, Tadahiro Numakawa, Kazuhiro Shimazu, et al. "BDNF-induced recruitment of TrkB receptor into neuronal lipid rafts." Journal of Cell Biology 167, no. 6 (2004): 1205–15. http://dx.doi.org/10.1083/jcb.200404106.

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Brain-derived neurotrophic factor (BDNF) plays an important role in synaptic plasticity but the underlying signaling mechanisms remain unknown. Here, we show that BDNF rapidly recruits full-length TrkB (TrkB-FL) receptor into cholesterol-rich lipid rafts from nonraft regions of neuronal plasma membranes. Translocation of TrkB-FL was blocked by Trk inhibitors, suggesting a role of TrkB tyrosine kinase in the translocation. Disruption of lipid rafts by depleting cholesterol from cell surface blocked the ligand-induced translocation. Moreover, disruption of lipid rafts prevented potentiating effe

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Wójcik-Gryciuk, Anna, Olga Gajewska-Woźniak, Katarzyna Kordecka, Paweł M. Boguszewski, Wioletta Waleszczyk, and Małgorzata Skup. "Neuroprotection of Retinal Ganglion Cells with AAV2-BDNF Pretreatment Restoring Normal TrkB Receptor Protein Levels in Glaucoma." International Journal of Molecular Sciences 21, no. 17 (2020): 6262. http://dx.doi.org/10.3390/ijms21176262.

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Intravitreal delivery of brain-derived neurotrophic factor (BDNF) by injection of recombinant protein or by gene therapy can alleviate retinal ganglion cell (RGC) loss after optic nerve injury (ONI) or laser-induced ocular hypertension (OHT). In models of glaucoma, BDNF therapy can delay or halt RGCs loss, but this protection is time-limited. The decreased efficacy of BDNF supplementation has been in part attributed to BDNF TrkB receptor downregulation. However, whether BDNF overexpression causes TrkB downregulation, impairing long-term BDNF signaling in the retina, has not been conclusively p

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13

Martin, Mauricio G., Simona Perga, Laura Trovò, et al. "Cholesterol Loss Enhances TrkB Signaling in Hippocampal Neurons Aging in Vitro." Molecular Biology of the Cell 19, no. 5 (2008): 2101–12. http://dx.doi.org/10.1091/mbc.e07-09-0897.

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Binding of the neurotrophin brain-derived neurotrophic factor (BDNF) to the TrkB receptor is a major survival mechanism during embryonic development. In the aged brain, however, BDNF levels are low, suggesting that if TrkB is to play a role in survival at this stage additional mechanisms must have developed. We here show that TrkB activity is most robust in the hippocampus of 21-d-old BDNF-knockout mice as well as in old, wild-type, and BDNF heterozygous animals. Moreover, robust TrkB activity is evident in old but not young hippocampal neurons differentiating in vitro in the absence of any ex

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14

Hang, Peng-Zhou, Hua Zhu, Pei-Feng Li, et al. "The Emerging Role of BDNF/TrkB Signaling in Cardiovascular Diseases." Life 11, no. 1 (2021): 70. http://dx.doi.org/10.3390/life11010070.

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Brain-derived neurotrophic factor (BDNF) is one of the most abundant neurotrophins in the central nervous system. Numerous studies suggest that BDNF has extensive roles by binding to its specific receptor, tropomyosin-related kinase receptor B (TrkB), and thereby triggering downstream signaling pathways. Recently, growing evidence highlights that the BDNF/TrkB pathway is expressed in the cardiovascular system and closely associated with the development and outcome of cardiovascular diseases (CVD), including coronary artery disease, heart failure, cardiomyopathy, hypertension, and metabolic dis

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15

Sopi, Ramadan B., Richard J. Martin, Musa A. Haxhiu, et al. "Role of brain-derived neurotrophic factor in hyperoxia-induced enhancement of contractility and impairment of relaxation in lung parenchyma." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 2 (2008): L348—L355. http://dx.doi.org/10.1152/ajplung.00067.2008.

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Prolonged hyperoxic exposure contributes to neonatal lung injury, and airway hyperreactivity is characterized by enhanced contraction and impaired relaxation of airway smooth muscle. Our previous data demonstrate that hyperoxia in rat pups upregulates expression of brain-derived neurotrophic factor (BDNF) mRNA and protein, disrupts NO-cGMP signaling, and impairs cAMP production in airway smooth muscle. We hypothesized that BDNF-tyrosine kinase B (TrkB) signaling plays a functional role in airway hyperreactivity via upregulation of cholinergic mechanisms in hyperoxia-exposed lungs. Five-day-old

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16

Jensen, T., and A. L. Johnson. "Expression and function of brain-derived neurotrophin factor and its receptor, TrkB, in ovarian follicles from the domestic hen (Gallus gallus domesticus)." Journal of Experimental Biology 204, no. 12 (2001): 2087–95. http://dx.doi.org/10.1242/jeb.204.12.2087.

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SUMMARY This report summarizes patterns of mRNA expression for the brain-derived neurotrophic factor (BDNF) together with its high-affinity neurotrophin receptor trkB within the hen ovary during follicle development, describes hormonal mechanisms for the regulation of trkB gene expression and provides preliminary evidence for a novel function for BDNF-mediated TrkB signaling within the granulosa layer. Levels of BDNF mRNA in the thecal layer and of trkB mRNA within the granulosa cell layer increase coincident with entrance of the follicle into the preovulatory hierarchy. Localization of the BD

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Bariohay, Bruno, Julien Roux, Catherine Tardivel, Jérôme Trouslard, Andre Jean, and Bruno Lebrun. "Brain-Derived Neurotrophic Factor/Tropomyosin-Related Kinase Receptor Type B Signaling Is a Downstream Effector of the Brainstem Melanocortin System in Food Intake Control." Endocrinology 150, no. 6 (2009): 2646–53. http://dx.doi.org/10.1210/en.2008-1184.

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It has been shown that the neurotropin brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin-related kinase receptor type B (TrkB), contribute to the central control of food intake. BDNF has previously been implicated as a probable downstream effector of melanocortinergic signaling within the ventromedial hypothalamus, and we have shown its implication as an anorexigenic factor within the brainstem autonomic integrator of food intake control, namely the dorsal vagal complex (DVC). In the brainstem, the melanocortinergic signaling pathway is known to integrate pha

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Olenick, Mara A., Roberto Dominguez, and Erika L. F. Holzbaur. "Dynein activator Hook1 is required for trafficking of BDNF-signaling endosomes in neurons." Journal of Cell Biology 218, no. 1 (2018): 220–33. http://dx.doi.org/10.1083/jcb.201805016.

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Axonal transport is required for neuronal development and survival. Transport from the axon to the soma is driven by the molecular motor cytoplasmic dynein, yet it remains unclear how dynein is spatially and temporally regulated. We find that the dynein effector Hook1 mediates transport of TrkB–BDNF-signaling endosomes in primary hippocampal neurons. Hook1 comigrates with a subpopulation of Rab5 endosomes positive for TrkB and BDNF, which exhibit processive retrograde motility with faster velocities than the overall Rab5 population. Knockdown of Hook1 significantly reduced the motility of BDNF

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Numakawa, Tadahiro, and Haruki Odaka. "Brain-Derived Neurotrophic Factor Signaling in the Pathophysiology of Alzheimer’s Disease: Beneficial Effects of Flavonoids for Neuroprotection." International Journal of Molecular Sciences 22, no. 11 (2021): 5719. http://dx.doi.org/10.3390/ijms22115719.

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The function of the brain-derived neurotrophic factor (BDNF) via activation through its high-affinity receptor Tropomyosin receptor kinase B (TrkB) has a pivotal role in cell differentiation, cell survival, synaptic plasticity, and both embryonic and adult neurogenesis in central nervous system neurons. A number of studies have demonstrated the possible involvement of altered expression and action of the BDNF/TrkB signaling in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD). In this review, we introduce an essential role of the BDNF and its downstream signali

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Shang, Yingchun, Xin Wang, Fangjuan Li, Tao Yin, Jianhai Zhang, and Tao Zhang. "rTMS Ameliorates Prenatal Stress–Induced Cognitive Deficits in Male-Offspring Rats Associated With BDNF/TrkB Signaling Pathway." Neurorehabilitation and Neural Repair 33, no. 4 (2019): 271–83. http://dx.doi.org/10.1177/1545968319834898.

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Background. Growing evidences suggest that brain-derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) plays a key role in the regulation of hippocampal synaptic plasticity in a prenatal stress (PNS) rat model. Repetitive transcranial magnetic stimulation (rTMS) is currently being acknowledged to affect attention and memory in both preclinical and clinical studies, although the mechanism is still unclear. Objective. The current study aimed to explore whether a whole brain rTMS (5 Hz, 14 days) could ameliorate cognitive dysfunction–induced PNS in male offspring, and examine if t

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Al-Qudah, M., C. D. Anderson, S. Mahavadi, et al. "Brain-derived neurotrophic factor enhances cholinergic contraction of longitudinal muscle of rabbit intestine via activation of phospholipase C." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 4 (2014): G328—G337. http://dx.doi.org/10.1152/ajpgi.00203.2013.

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Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family of proteins best known for its role in neuronal survival, differentiation, migration, and synaptic plasticity in central and peripheral neurons. BDNF is also widely expressed in nonneuronal tissues including the gastrointestinal tract. The role of BDNF in intestinal smooth muscle contractility is not well defined. The aim of this study was to identify the role of BDNF in carbachol (CCh)- and substance P (SP)-induced contraction of intestinal longitudinal smooth muscle. BDNF, selective tropomyosin-related kinase B (TrkB

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Wu, Zhourui, Chun Chen, Seong Su Kang, et al. "Neurotrophic signaling deficiency exacerbates environmental risks for Alzheimer’s disease pathogenesis." Proceedings of the National Academy of Sciences 118, no. 25 (2021): e2100986118. http://dx.doi.org/10.1073/pnas.2100986118.

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The molecular mechanism of Alzheimer’s disease (AD) pathogenesis remains obscure. Life and/or environmental events, such as traumatic brain injury (TBI), high-fat diet (HFD), and chronic cerebral hypoperfusion (CCH), are proposed exogenous risk factors for AD. BDNF/TrkB, an essential neurotrophic signaling for synaptic plasticity and neuronal survival, are reduced in the aged brain and in AD patients. Here, we show that environmental factors activate C/EBPβ, an inflammatory transcription factor, which subsequently up-regulates δ-secretase that simultaneously cleaves both APP and Tau, triggerin

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Kawamura, Kazuhiro, Nanami Kawamura, Yuta Kawagoe, Jin Kumagai, Toshio Fujimoto, and Yukihiro Terada. "Suppression of Hydatidiform Molar Growth by Inhibiting Endogenous Brain-Derived Neurotrophic Factor/Tyrosine Kinase B Signaling." Endocrinology 153, no. 8 (2012): 3972–81. http://dx.doi.org/10.1210/en.2012-1167.

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Brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) receptor signaling promotes trophoblast growth in normal and abnormal pregnancy. It also regulates the growth of malignant trophoblastic, choriocarcinoma cells. However, possible involvement of this signaling system in hydatidiform mole, another major gestational trophoblastic disease, has not been determined. Here, we found the expression of BDNF in syncytiotrophoblasts and its receptor, TrkB, in cytotrophoblasts of hydatidiform mole using real-time RT-PCR and immunoassays. In molar explant cultures, treatment with soluble TrkB

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Lee, Heow Won, Monir Ahmad, Jonathan J. Weldrick, Hong-Wei Wang, Patrick G. Burgon, and Frans H. H. Leenen. "Effects of exercise training and TrkB blockade on cardiac function and BDNF-TrkB signaling postmyocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (2018): H1821—H1834. http://dx.doi.org/10.1152/ajpheart.00245.2018.

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Exercise training is beneficial for preserving cardiac function postmyocardial infarction (post-MI), but the underlying mechanisms are not well understood. We investigated one possible mechanism, brain-derived neurotrophic factor (BDNF)-tropomyosin-related kinase B (TrkB) signaling, with the TrkB blocker ANA-12 (0.5 mg·kg−1·day−1). Male Wistar rats underwent sham surgery or ligation of the left descending coronary artery. The surviving MI rats were allocated as follows: sedentary MI rats treated with vehicle, exercise-trained MI rats treated with vehicle, and exercise-trained MI rats treated w

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Cao, Maosheng, Qiaoge Niu, XinYu Xiang, et al. "Brain-Derived Neurotrophic Factor Regulates Ishikawa Cell Proliferation through the TrkB-ERK1/2 Signaling Pathway." Biomolecules 10, no. 12 (2020): 1645. http://dx.doi.org/10.3390/biom10121645.

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(1) Background: Endometrial regulation is a necessary condition for maintaining normal uterine physiology, which is driven by many growth factors. Growth factors produced in the endometrium are thought to be related to the proliferation of endometrial cells induced by estradiol-17β (E2). In this study, we found that E2 can induce the secretion of brain-derived neurotrophic factor (BDNF) in Ishikawa cells (the cells of an endometrial cell line). Furthermore, Ishikawa cells were used in exploring the regulatory role of BDNF in endometrial cells and to clarify the potential mechanism. (2) Methods

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Ottem, Erich N., Laurel A. Beck, Cynthia L. Jordan, and S. Marc Breedlove. "Androgen-Dependent Regulation of Brain-Derived Neurotrophic Factor and Tyrosine Kinase B in the Sexually Dimorphic Spinal Nucleus of the Bulbocavernosus." Endocrinology 148, no. 8 (2007): 3655–65. http://dx.doi.org/10.1210/en.2007-0308.

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Castration of adult male rats causes the dendrites of androgen-sensitive motoneurons of the spinal nucleus of the bulbocavernosus (SNB) to retract. Brain-derived neurotrophic factor (BDNF), via activation of tyrosine receptor kinase B (trkB), has been implicated in mediating androgen effects on SNB dendrites. We used in situ hybridization to demonstrate that SNB motoneurons in gonadally intact adult male rats contain mRNA for both BDNF and trkB. Two weeks after gonadectomy, both transcripts were significantly decreased in SNB motoneurons but not in the non-androgen-responsive motoneurons of th

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Tan, Shawn, Yixin Xiao, Henry H. Yin, Albert I. Chen, Tuck Wah Soong, and H. Shawn Je. "Postnatal TrkB ablation in corticolimbic interneurons induces social dominance in male mice." Proceedings of the National Academy of Sciences 115, no. 42 (2018): E9909—E9915. http://dx.doi.org/10.1073/pnas.1812083115.

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The tight balance between synaptic excitation and inhibition (E/I) within neocortical circuits in the mammalian brain is important for complex behavior. Many loss-of-function studies have demonstrated that brain-derived neurotrophic factor (BDNF) and its cognate receptor tropomyosin receptor kinase B (TrkB) are essential for the development of inhibitory GABAergic neurons. However, behavioral consequences of impaired BDNF/TrkB signaling in GABAergic neurons remain unclear, largely due to confounding motor function deficits observed in previous animal models. In this study, we generated conditi

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Agosto-Marlin, Ibis M., та Gordon S. Mitchell. "Spinal BDNF-induced phrenic motor facilitation requires PKCθ activity". Journal of Neurophysiology 118, № 5 (2017): 2755–62. http://dx.doi.org/10.1152/jn.00945.2016.

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Spinal brain-derived neurotrophic factor (BDNF) is necessary and sufficient for certain forms of long-lasting phrenic motor facilitation (pMF). BDNF elicits pMF by binding to its high-affinity receptor, tropomyosin receptor kinase B (TrkB), on phrenic motor neurons, potentially activating multiple downstream signaling cascades. Canonical BDNF/TrkB signaling includes the 1) Ras/RAF/MEK/ERK MAP kinase, 2) phosphatidylinositol 3‐kinase (PI3K)/Akt, and 3) PLCγ/PKC pathways. Here we demonstrate that spinal BDNF-induced pMF requires PLCγ/PKCθ in normal rats but not MEK/ERK or PI3K/Akt signaling. Cer

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Li, Yun, Daishi Yui, Bryan W. Luikart, et al. "Conditional ablation of brain-derived neurotrophic factor-TrkB signaling impairs striatal neuron development." Proceedings of the National Academy of Sciences 109, no. 38 (2012): 15491–96. http://dx.doi.org/10.1073/pnas.1212899109.

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Neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), are associated with the physiology of the striatum and the loss of its normal functioning under pathological conditions. The role of BDNF and its downstream signaling in regulating the development of the striatum has not been fully investigated, however. Here we report that ablation of Bdnf in both the cortex and substantia nigra depletes BDNF in the striatum, and leads to impaired striatal development, severe motor deficits, and postnatal lethality. Furthermore, striatal-specific ablation of TrkB, the gene encoding the hi

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Andreska, Thomas, Patrick Lüningschrör, and Michael Sendtner. "Regulation of TrkB cell surface expression—a mechanism for modulation of neuronal responsiveness to brain-derived neurotrophic factor." Cell and Tissue Research 382, no. 1 (2020): 5–14. http://dx.doi.org/10.1007/s00441-020-03224-7.

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Abstract Neurotrophin signaling via receptor tyrosine kinases is essential for the development and function of the nervous system in vertebrates. TrkB activation and signaling show substantial differences to other receptor tyrosine kinases of the Trk family that mediate the responses to nerve growth factor and neurotrophin-3. Growing evidence suggests that TrkB cell surface expression is highly regulated and determines the sensitivity of neurons to brain-derived neurotrophic factor (BDNF). This translocation of TrkB depends on co-factors and modulators of cAMP levels, N-glycosylation, and rece

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McCarthy, Deirdre M., Genevieve A. Bell, Elisa N. Cannon, et al. "Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model." Developmental Neuroscience 38, no. 5 (2016): 354–64. http://dx.doi.org/10.1159/000452739.

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Prenatal cocaine exposure remains a major public health concern because of its adverse impact on cognitive function in children and adults. We report that prenatal cocaine exposure produces significant deficits in reversal learning, a key component of cognitive flexibility, in a mouse model. We used an olfactory reversal learning paradigm and found that the prenatally cocaine-exposed mice showed a marked failure to learn the reversed paradigm. Because brain-derived neurotrophic factor (BDNF) is a key regulator of cognitive functions, and because prenatal cocaine exposure increases the expressi

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Rivera, Claudio, Hong Li, Judith Thomas-Crusells, et al. "BDNF-induced TrkB activation down-regulates the K+–Cl− cotransporter KCC2 and impairs neuronal Cl− extrusion." Journal of Cell Biology 159, no. 5 (2002): 747–52. http://dx.doi.org/10.1083/jcb.200209011.

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Pathophysiological activity and various kinds of traumatic insults are known to have deleterious long-term effects on neuronal Cl− regulation, which can lead to a suppression of fast postsynaptic GABAergic responses. Brain-derived neurotrophic factor (BDNF) increases neuronal excitability through a conjunction of mechanisms that include regulation of the efficacy of GABAergic transmission. Here, we show that exposure of rat hippocampal slice cultures and acute slices to exogenous BDNF or neurotrophin-4 produces a TrkB-mediated fall in the neuron-specific K+–Cl− cotransporter KCC2 mRNA and prot

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Hoffman, M. S., N. L. Nichols, P. M. Macfarlane, and G. S. Mitchell. "Phrenic long-term facilitation after acute intermittent hypoxia requires spinal ERK activation but not TrkB synthesis." Journal of Applied Physiology 113, no. 8 (2012): 1184–93. http://dx.doi.org/10.1152/japplphysiol.00098.2012.

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Acute intermittent hypoxia (AIH) elicits a form of spinal respiratory plasticity known as phrenic long-term facilitation (pLTF). pLTF requires spinal serotonin receptor-2 activation, the synthesis of new brain-derived neurotrophic factor (BDNF), and the activation of its high-affinity receptor tyrosine kinase, TrkB. Spinal adenosine 2A receptor activation elicits a distinct pathway to phrenic motor facilitation (pMF); this BDNF synthesis-independent pathway instead requires new synthesis of an immature TrkB isoform. Since hypoxia increases extracellular adenosine levels, we tested the hypothes

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Stucky, Andres, Kalindi P. Bakshi, Eitan Friedman, and Hoau-Yan Wang. "Prenatal Cocaine Exposure Upregulates BDNF-TrkB Signaling." PLOS ONE 11, no. 8 (2016): e0160585. http://dx.doi.org/10.1371/journal.pone.0160585.

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Pandya, Chirayu D., Ammar Kutiyanawalla, and Anilkumar Pillai. "BDNF–TrkB signaling and neuroprotection in schizophrenia." Asian Journal of Psychiatry 6, no. 1 (2013): 22–28. http://dx.doi.org/10.1016/j.ajp.2012.08.010.

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Anderson, Ethan M., Anne Marie Wissman, Joyce Chemplanikal, et al. "BDNF-TrkB controls cocaine-induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors." Proceedings of the National Academy of Sciences 114, no. 35 (2017): 9469–74. http://dx.doi.org/10.1073/pnas.1702441114.

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Chronic cocaine use is associated with prominent morphological changes in nucleus accumbens shell (NACsh) neurons, including increases in dendritic spine density along with enhanced motivation for cocaine, but a functional relationship between these morphological and behavioral phenomena has not been shown. Here we show that brain-derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for cocaine-induced dendritic spine formation by using either localized TrkB knockout or viral-mediated expression of a dominant negative, kinase-dea

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Boukhatem, Imane, Samuel Fleury, Melanie Welman, et al. "The brain-derived neurotrophic factor prompts platelet aggregation and secretion." Blood Advances 5, no. 18 (2021): 3568–80. http://dx.doi.org/10.1182/bloodadvances.2020004098.

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Abstract Brain-derived neurotrophic factor (BDNF) has both autocrine and paracrine roles in neurons, and its release and signaling mechanisms have been extensively studied in the central nervous system. Large quantities of BDNF have been reported in circulation, essentially stored in platelets with concentrations reaching 100- to 1000-fold those of neurons. Despite this abundance, the function of BDNF in platelet biology has not been explored. At low concentrations, BDNF primed platelets, acting synergistically with classical agonists. At high concentrations, BDNF induced complete biphasic pla

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Mitre, Mariela, Abigail Mariga, and Moses V. Chao. "Neurotrophin signalling: novel insights into mechanisms and pathophysiology." Clinical Science 131, no. 1 (2016): 13–23. http://dx.doi.org/10.1042/cs20160044.

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Neurotrophins, such as brain-derived neurotrophic factor (BDNF), are prominent regulators of neuronal survival, growth and differentiation during development. While trophic factors are viewed as well-understood but not innovative molecules, there are many lines of evidence indicating that BDNF plays an important role in the pathophysiology of many neurodegenerative disorders, depression, anxiety and other psychiatric disorders. In particular, lower levels of BDNF are associated with the aetiology of Alzheimer's and Huntington's diseases. A major challenge is to explain how neurotrophins are ab

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Li, Xiaohong, Chong Chen, Xiping Yang, et al. "Acupuncture Improved Neurological Recovery after Traumatic Brain Injury by Activating BDNF/TrkB Pathway." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/8460145.

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How to promote neural repair following traumatic brain injury (TBI) has long been an intractable problem. Although acupuncture has been demonstrated to facilitate the neurological recovery, the underlying mechanism is elusive. Brain-derived neurotrophic factor (BDNF) exerts substantial protective effects for neurological disorders. In this study, we found that the level of BDNF and tropomyosin receptor kinase B (TrkB) was elevated spontaneously after TBI and reached up to the peak at 12 h. Nevertheless, this enhancement is quickly declined to the normal at 48 h. After combined stimulation at t

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Wang, Hua, Yuan Wei, Yichen Pu, et al. "Brain-derived neurotrophic factor stimulation of T-type Ca2+ channels in sensory neurons contributes to increased peripheral pain sensitivity." Science Signaling 12, no. 600 (2019): eaaw2300. http://dx.doi.org/10.1126/scisignal.aaw2300.

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Although brain-derived neurotrophic factor (BDNF) is implicated in the nociceptive signaling of peripheral sensory neurons, the underlying mechanisms remain largely unknown. Here, we elucidated the effects of BDNF on the neuronal excitability of trigeminal ganglion (TG) neurons and the pain sensitivity of rats mediated by T-type Ca2+ channels. BDNF reversibly and dose-dependently enhanced T-type channel currents through the activation of tropomyosin receptor kinase B (TrkB). Antagonism of phosphatidylinositol 3-kinase (PI3K) but not of its downstream target, the kinase AKT, abolished the BDNF-

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Hu, Min, Wei Zou, Chun-Yan Wang, et al. "Hydrogen Sulfide Protects against Chronic Unpredictable Mild Stress-Induced Oxidative Stress in Hippocampus by Upregulation of BDNF-TrkB Pathway." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/2153745.

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Chronic unpredictable mild stress (CUMS) induces hippocampal oxidative stress. H2S functions as a neuroprotectant against oxidative stress in brain. We have previously shown the upregulatory effect of H2S on BDNF protein expression in the hippocampus of rats. Therefore, we hypothesized that H2S prevents CUMS-generated oxidative stress by upregulation of BDNF-TrkB pathway. We showed that NaHS (0.03 or 0.1 mmol/kg/day) ameliorates the level of hippocampal oxidative stress, including reduced levels of malondialdehyde (MDA) and 4-hydroxy-2-trans-nonenal (4-HNE), as well as increased level of gluta

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Bariohay, Bruno, Catherine Tardivel, Juliette Pio, André Jean, and Bernadette Félix. "BDNF-TrkB signaling interacts with the GABAergic system to inhibit rhythmic swallowing in the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 4 (2008): R1050—R1059. http://dx.doi.org/10.1152/ajpregu.90407.2008.

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Brain-derived neurotrophic factor (BDNF) acts as an anorexigenic factor in the dorsal vagal complex (DVC) of the adult rat brain stem. The DVC contains the premotoneurons controlling swallowing, a motor component of feeding behavior. Although rats with transected midbrain do not seek out food, they are able to swallow and to ingest food. Because BDNF and tropomyosin-related kinase B (TrkB) receptors are expressed in the DVC, this study hypothesized that BDNF could modify the activity of premotoneurons involved in swallowing. Repetitive electrical stimulation of the superior laryngeal nerve (SL

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Numakawa, Tadahiro, Haruki Odaka, and Naoki Adachi. "Actions of Brain-Derived Neurotrophin Factor in the Neurogenesis and Neuronal Function, and Its Involvement in the Pathophysiology of Brain Diseases." International Journal of Molecular Sciences 19, no. 11 (2018): 3650. http://dx.doi.org/10.3390/ijms19113650.

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It is well known that brain-derived neurotrophic factor, BDNF, has an important role in a variety of neuronal aspects, such as differentiation, maturation, and synaptic function in the central nervous system (CNS). BDNF stimulates mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), phosphoinositide-3kinase (PI3K), and phospholipase C (PLC)-gamma pathways via activation of tropomyosin receptor kinase B (TrkB), a high affinity receptor for BDNF. Evidence has shown significant contributions of these signaling pathways in neurogenesis and synaptic plasticity in in vi

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Sandhya, Varot K., Rajesh Raju, Renu Verma, et al. "A network map of BDNF/TRKB and BDNF/p75NTR signaling system." Journal of Cell Communication and Signaling 7, no. 4 (2013): 301–7. http://dx.doi.org/10.1007/s12079-013-0200-z.

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Rössler, Oliver G., and Gerald Thiel. "Brain-derived neurotrophic factor-, epidermal growth factor-, or A-Raf-induced growth of HaCaT keratinocytes requires extracellular signal-regulated kinase." American Journal of Physiology-Cell Physiology 286, no. 5 (2004): C1118—C1129. http://dx.doi.org/10.1152/ajpcell.00301.2003.

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The epidermal growth factor (EGF) receptor plays an important role in epithelial cells by controlling cell proliferation and survival. Keratinocytes also express another class of receptor tyrosine kinases, the neurotrophin receptors. To analyze the biological role of the neurotrophin brain-derived neurotrophic factor (BDNF) in keratinocytes, we expressed the BDNF receptor TrkB in immortalized human HaCaT keratinocytes. Stimulation of HaCaT-TrkB cells with BDNF induced DNA synthesis and increased mitochondrial reduction capacities, both indications of proliferating cells. An analysis of the sig

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Fukumoto, Kenichi, Manoela V. Fogaça, Rong-Jian Liu, et al. "Activity-dependent brain-derived neurotrophic factor signaling is required for the antidepressant actions of (2R,6R)-hydroxynorketamine." Proceedings of the National Academy of Sciences 116, no. 1 (2018): 297–302. http://dx.doi.org/10.1073/pnas.1814709116.

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Ketamine, a noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist, produces rapid and long-lasting antidepressant effects in major depressive disorder (MDD) patients. (2R,6R)-Hydroxynorketamine [(2R,6R)-HNK], a metabolite of ketamine, is reported to produce rapid antidepressant effects in rodent models without the side effects of ketamine. Importantly, (2R,6R)-HNK does not block NMDA receptors like ketamine, and the molecular signaling mechanisms for (2R,6R)-HNK remain unknown. Here, we examined the involvement of BDNF/TrkB/mechanistic target of rapamycin complex 1 (mTORC1) signaling

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Lee, Young-Ju, Hye Ryeong Kim, Chang Youn Lee, et al. "2-Phenylethylamine (PEA) Ameliorates Corticosterone-Induced Depression-Like Phenotype via the BDNF/TrkB/CREB Signaling Pathway." International Journal of Molecular Sciences 21, no. 23 (2020): 9103. http://dx.doi.org/10.3390/ijms21239103.

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Depression is a serious medical illness that is one of the most prevalent psychiatric disorders. Corticosterone (CORT) increases depression-like behavior, with some effects on anxiety-like behavior. 2-Phenethylamine (PEA) is a monoamine alkaloid that acts as a central nervous system stimulant in humans. Here, we show that PEA exerts antidepressant effects by modulating the Brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element binding protein (CREB) signaling pathway in CORT-induced depression. To investigate the potential effects of PEA on CORT-ind

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Zhao, Liangfang, and Eric S. Levine. "BDNF-endocannabinoid interactions at neocortical inhibitory synapses require phospholipase C signaling." Journal of Neurophysiology 111, no. 5 (2014): 1008–15. http://dx.doi.org/10.1152/jn.00554.2013.

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Endogenous cannabinoids (endocannabinoids) and neurotrophins, particularly brain-derived neurotrophic factor (BDNF), are potent synaptic modulators that are expressed throughout the forebrain and play critical roles in many behavioral processes. Although the effects of BDNF at excitatory synapses have been well characterized, the mechanisms of action of BDNF at inhibitory synapses are not well understood. Previously we have found that BDNF suppresses presynaptic GABA release in layer 2/3 of the neocortex via postsynaptic tropomyosin-related kinase receptor B (trkB) receptor-induced release of

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Schaich, Chris L., Theresa L. Wellman, Zachary Einwag, Richard A. Dutko, and Benedek Erdos. "Inhibition of BDNF signaling in the paraventricular nucleus of the hypothalamus lowers acute stress-induced pressor responses." Journal of Neurophysiology 120, no. 2 (2018): 633–43. http://dx.doi.org/10.1152/jn.00459.2017.

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Brain-derived neurotrophic factor (BDNF) expression increases in the paraventricular nucleus of the hypothalamus (PVN) during stress, and our recent studies indicate that BDNF induces sympathoexcitatory and hypertensive responses when injected acutely or overexpressed chronically in the PVN. However, it remained to be investigated whether BDNF is involved in the mediation of stress-induced cardiovascular responses. Here we tested the hypothesis that inhibition of the high-affinity BDNF receptor TrkB in the PVN diminishes acute stress-induced cardiovascular responses. Male Sprague-Dawley rats w

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Roesler, Rafael, Caroline Brunetto de Farias, Ana Lucia Abujamra, Algemir Lunardi Brunetto, and Gilberto Schwartsmann. "BDNF/TrkB signaling as an anti-tumor target." Expert Review of Anticancer Therapy 11, no. 10 (2011): 1473–75. http://dx.doi.org/10.1586/era.11.150.

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