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  • 1
    Online Resource
    Online Resource
    BDNF-based synaptic repair as a disease-modifying strategy for neurodegenerative diseases
    Springer Science and Business Media LLC ; 2013
    In:  Nature Reviews Neuroscience Vol. 14, No. 6 ( 2013-6), p. 401-416
    Details
    In: Nature Reviews Neuroscience, Springer Science and Business Media LLC, Vol. 14, No. 6 ( 2013-6), p. 401-416
    Type of Medium: Online Resource
    ISSN: 1471-003X , 1471-0048
    URL: Article
    DOI: 10.1038/nrn3505
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2013
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    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Neuronal release of proBDNF
    Springer Science and Business Media LLC ; 2009
    In:  Nature Neuroscience Vol. 12, No. 2 ( 2009-2), p. 113-115
    Details
    In: Nature Neuroscience, Springer Science and Business Media LLC, Vol. 12, No. 2 ( 2009-2), p. 113-115
    Type of Medium: Online Resource
    ISSN: 1097-6256 , 1546-1726
    URL: Article
    DOI: 10.1038/nn.2244
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2009
    detail.hit.zdb_id: 1420596-8
    detail.hit.zdb_id: 1494955-6
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Pro-BDNF–induced synaptic depression and retraction at developing neuromuscular synapses
    Rockefeller University Press ; 2009
    In:  Journal of Cell Biology Vol. 185, No. 4 ( 2009-05-18), p. 727-741
    Details
    In: Journal of Cell Biology, Rockefeller University Press, Vol. 185, No. 4 ( 2009-05-18), p. 727-741
    Abstract: Postsynaptic cells generate positive and negative signals that retrogradely modulate presynaptic function. At developing neuromuscular synapses, prolonged stimulation of muscle cells induces sustained synaptic depression. We provide evidence that pro–brain-derived neurotrophic factor (BDNF) is a negative retrograde signal that can be converted into a positive signal by metalloproteases at the synaptic junctions. Application of pro-BDNF induces a dramatic decrease in synaptic efficacy followed by a retraction of presynaptic terminals, and these effects are mediated by presynaptic pan-neurotrophin receptor p75 (p75NTR), the pro-BDNF receptor. A brief stimulation of myocytes expressing cleavable or uncleavable pro-BDNF elicits synaptic potentiation or depression, respectively. Extracellular application of metalloprotease inhibitors, which inhibits the cleavage of endogenous pro-BDNF, facilitates the muscle stimulation–induced synaptic depression. Inhibition of presynaptic p75NTR or postsynaptic BDNF expression also blocks the activity-dependent synaptic depression and retraction. These results support a model in which postsynaptic secretion of a single molecule, pro-BDNF, may stabilize or eliminate presynaptic terminals depending on its proteolytic conversion at the synapses.
    Type of Medium: Online Resource
    ISSN: 1540-8140 , 0021-9525
    URL: Article
    DOI: 10.1083/jcb.200811147
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2009
    detail.hit.zdb_id: 1421310-2
    detail.hit.zdb_id: 218154-X
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Differential effects of transient and sustained activation of BDNF‐TrkB signaling
    Wiley ; 2018
    In:  Developmental Neurobiology Vol. 78, No. 7 ( 2018-07), p. 647-659
    Details
    In: Developmental Neurobiology, Wiley, Vol. 78, No. 7 ( 2018-07), p. 647-659
    Abstract: Brain‐derived neurotrophic factor (BDNF) serves a pleiotropic role in the central nervous system, ranging from promoting neuronal survival and differentiation during development and synaptic modulation in the adult. An important, yet unanswered question is how BDNF could serve such diverse functions, sometimes in the same cell. At least two modes of BDNF actions have been elucidated so far based on BDNF signaling kinetics and/or the activity status of the responding neurons. Acute and gradual increases in extracellular BDNF concentrations elicit, respectively, transient and sustained activation of TrkB receptor and its downstream signaling, leading to differential molecular and cellular functions. In cultured neurons, sustained TrkB activation promotes neuronal dendritic arborization and spinogenesis, whereas transient TrkB activation facilitates dendritic growth and spine morphogenesis. In hippocampal slices, slow delivery of BDNF facilitates LTP, whereas fast application of BDNF enhances basal synaptic transmission in schaffer collateral synapses. High‐frequency stimulation of neurons converts BDNF‐induced TrkB signaling from a transient to a sustained mode. These initial insights lay the foundation for future investigation of the BDNF‐TrkB pathway, and analogous signaling pathways to gain a comprehensive understanding to enable translational research. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 78: 647–659, 2018
    Type of Medium: Online Resource
    ISSN: 1932-8451 , 1932-846X
    URL: Issue
    URL: Article
    DOI: 10.1002/dneu.v78.7
    DOI: 10.1002/dneu.22592
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2256184-5
    detail.hit.zdb_id: 2266191-8
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  • 5
    Online Resource
    Online Resource
    Alternative splicing of human metabotropic glutamate receptor 3
    Wiley ; 2006
    In:  Journal of Neurochemistry Vol. 96, No. 4 ( 2006-02), p. 1139-1148
    Details
    In: Journal of Neurochemistry, Wiley, Vol. 96, No. 4 ( 2006-02), p. 1139-1148
    Abstract: The metabotropic glutamate receptor 3 (GRM3, mGluR3) is important in regulating synaptic glutamate. Here, we report the existence of three splice variants of GRM3 in human brain arising from exon skipping events. The transcripts are expressed in prefrontal cortex, hippocampus and cerebellum, and in B lymphoblasts. We found no evidence for alternative splicing of GRM2. The most abundant GRM3 variant lacks exon 4 (GRM3Δ4). In silico translation analysis of GRM3Δ4 predicts a truncated protein with a conserved extracellular ligand binding domain, absence of a seven‐transmembrane domain, and a unique 96‐amino acid C‐terminus. When expressed in rat hippocampal neurons, GRM3Δ4 is translated into a 60 kDa protein. Immunostaining and cell fractionation data indicate that the truncated protein is primarily membrane‐associated. An antibody developed against the GRM3Δ4 C‐terminus detects a protein of approximately 60 kDa in human brain lysates and in B lymphoblasts, suggesting translation of GRM3Δ4 in vivo . The existence of the GRM3Δ4 isoform is relevant in the light of the reported association of non‐coding single nucleotide polymorphisms (SNPs) in GRM3 with schizophrenia, and with the potential of GRM3 as a therapeutic target for several neuropsychiatric disorders.
    Type of Medium: Online Resource
    ISSN: 0022-3042 , 1471-4159
    URL: Issue
    URL: Article
    DOI: 10.1111/jnc.2006.96.issue-4
    DOI: 10.1111/j.1471-4159.2005.03609.x
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 80158-6
    detail.hit.zdb_id: 2020528-4
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  • 6
    Online Resource
    Online Resource
    ProNGF promotes neurite growth from a subset of NGF-dependent neurons by a p75NTR-dependent mechanism
    The Company of Biologists ; 2013
    In:  Development Vol. 140, No. 10 ( 2013-05-15), p. 2108-2117
    Details
    In: Development, The Company of Biologists, Vol. 140, No. 10 ( 2013-05-15), p. 2108-2117
    Abstract: The somatosensory and sympathetic innervation of the vertebrate head is derived principally from the neurons of trigeminal and superior cervical ganglia (SCG), respectively. During development, the survival of both populations of neurons and the terminal growth and branching of their axons in the tissues they innervate is regulated by the supply of nerve growth factor (NGF) produced by these tissues. NGF is derived by proteolytic cleavage of a large precursor protein, proNGF, which is recognised to possess distinctive biological functions. Here, we show that proNGF promotes profuse neurite growth and branching from cultured postnatal mouse SCG neurons. In marked contrast, proNGF does not promote the growth of trigeminal neurites. Studies using compartment cultures demonstrated that proNGF acts locally on SCG neurites to promote growth. The neurite growth-promoting effect of proNGF is not observed in SCG neurons cultured from p75NTR-deficient mice, and proNGF does not phosphorylate the NGF receptor tyrosine kinase TrkA. These findings suggest that proNGF selectively promotes the growth of neurites from a subset of NGF-responsive neurons by a p75NTR-dependent mechanism during postnatal development when the axons of these neurons are ramifying within their targets in vivo.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.085266
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2013
    detail.hit.zdb_id: 1411623-6
    detail.hit.zdb_id: 2007916-3
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  • 7
    Online Resource
    Online Resource
    Ama“Zinc” Link between TrkB Transactivation and Synaptic Plasticity
    Elsevier BV ; 2008
    In:  Neuron Vol. 57, No. 4 ( 2008-02), p. 477-479
    Details
    In: Neuron, Elsevier BV, Vol. 57, No. 4 ( 2008-02), p. 477-479
    Type of Medium: Online Resource
    ISSN: 0896-6273
    URL: Article
    DOI: 10.1016/j.neuron.2008.02.004
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
    detail.hit.zdb_id: 808167-0
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  • 8
    Online Resource
    Online Resource
    Control of extracellular cleavage of ProBDNF by high frequency neuronal activity
    Proceedings of the National Academy of Sciences ; 2009
    In:  Proceedings of the National Academy of Sciences Vol. 106, No. 4 ( 2009-01-27), p. 1267-1272
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 106, No. 4 ( 2009-01-27), p. 1267-1272
    Abstract: Pro- and mature neurotrophins often elicit opposing biological effects. For example, mature brain-derived neurotrophic factor (mBDNF) is critical for long-term potentiation induced by high-frequency stimulation, whereas proBDNF facilitate long-term depression induced by low-frequency stimulation. Because mBDNF is derived from proBDNF by endoproteolytic cleavage, mechanisms regulating the cleavage of proBDNF may control the direction of BDNF regulation. Using methods that selectively detect proBDNF or mBDNF, we show that low-frequency stimulation induced predominant proBDNF secretion in cultured hippocampal neurons. In contrast, high-frequency stimulation preferentially increased extracellular mBDNF. Inhibition of extracellular, but not intracellular cleavage of proBDNF greatly reduced high-frequency stimulation-induced extracellular mBDNF. Moreover, high-frequency, but not low-frequency stimulation selectively induced the secretion of tissue plasminogen activator, a key protease involved in extracellular proBDNF to mBDNF conversion. Thus, high-frequency neuronal activity controls the ratio of extracellular proBDNF/mBDNF by regulating the secretion of extracellular proteases. Our study demonstrates activity-dependent control of extracellular proteolytic cleavage of a secretory protein, and reveals an important mechanism that controls diametrically opposed functions of BDNF isoforms.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0807322106
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2009
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
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  • 9
    Online Resource
    Online Resource
    Role of pro-brain-derived neurotrophic factor (proBDNF) to mature BDNF conversion in activity-dependent competition at developing neuromuscular synapses
    Proceedings of the National Academy of Sciences ; 2012
    In:  Proceedings of the National Academy of Sciences Vol. 109, No. 39 ( 2012-09-25), p. 15924-15929
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 109, No. 39 ( 2012-09-25), p. 15924-15929
    Abstract: Formation of specific neuronal connections often involves competition between adjacent axons, leading to stabilization of the active terminal, while retraction of the less active ones. The underlying molecular mechanisms remain unknown. We show that activity-dependent conversion of pro–brain-derived neurotrophic factor (proBDNF) to mature (m)BDNF mediates synaptic competition. Stimulation of motoneurons triggers proteolytic conversion of proBDNF to mBDNF at nerve terminals. In Xenopus nerve–muscle cocultures, in which two motoneurons innervate one myocyte, proBDNF-p75 NTR signaling promotes retraction of the less active terminal, whereas mBDNF–tyrosine-related kinase B (TrkB) p75NTR (p75 neurotrophin receptor) facilitates stabilization of the active one. Thus, proBDNF and mBDNF may serve as potential “punishment” and “reward” signals for inactive and active terminals, respectively, and activity-dependent conversion of proBDNF to mBDNF may regulate synapse elimination.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1207767109
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2012
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Chemically Inducible Inactivation of Protein Synthesis in Genetically Targeted Neurons
    Society for Neuroscience ; 2009
    In:  The Journal of Neuroscience Vol. 29, No. 21 ( 2009-05-27), p. 6761-6766
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 29, No. 21 ( 2009-05-27), p. 6761-6766
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1280-09.2009
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2009
    detail.hit.zdb_id: 1475274-8
    detail.hit.zdb_id: 604637-X
    SSG: 12
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