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  • 1
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    Secreted semaphorins control spine distribution and morphogenesis in the postnatal CNS (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-17
    Description: The majority of excitatory synapses in the mammalian CNS (central nervous system) are formed on dendritic spines, and spine morphology and distribution are critical for synaptic transmission, synaptic integration and plasticity. Here, we show that a secreted semaphorin, Sema3F, is a negative regulator of spine development and synaptic structure. Mice with null mutations in genes encoding Sema3F, and its holoreceptor components neuropilin-2 (Npn-2, also known as Nrp2) and plexin A3 (PlexA3, also known as Plxna3), exhibit increased dentate gyrus (DG) granule cell (GC) and cortical layer V pyramidal neuron spine number and size, and also aberrant spine distribution. Moreover, Sema3F promotes loss of spines and excitatory synapses in dissociated neurons in vitro, and in Npn-2(-/-) brain slices cortical layer V and DG GCs exhibit increased mEPSC (miniature excitatory postsynaptic current) frequency. In contrast, a distinct Sema3A-Npn-1/PlexA4 signalling cascade controls basal dendritic arborization in layer V cortical neurons, but does not influence spine morphogenesis or distribution. These disparate effects of secreted semaphorins are reflected in the restricted dendritic localization of Npn-2 to apical dendrites and of Npn-1 (also known as Nrp1) to all dendrites of cortical pyramidal neurons. Therefore, Sema3F signalling controls spine distribution along select dendritic processes, and distinct secreted semaphorin signalling events orchestrate CNS connectivity through the differential control of spine morphogenesis, synapse formation, and the elaboration of dendritic morphology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842559/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842559/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tran, Tracy S -- Rubio, Maria E -- Clem, Roger L -- Johnson, Dontais -- Case, Lauren -- Tessier-Lavigne, Marc -- Huganir, Richard L -- Ginty, David D -- Kolodkin, Alex L -- F32 NS051003/NS/NINDS NIH HHS/ -- P50 MH06883/MH/NIMH NIH HHS/ -- R01 DC-006881/DC/NIDCD NIH HHS/ -- R01 MH059199/MH/NIMH NIH HHS/ -- R01 MH059199-07/MH/NIMH NIH HHS/ -- R01 MH059199-08/MH/NIMH NIH HHS/ -- R01 MH059199-09/MH/NIMH NIH HHS/ -- R01 MH059199-10/MH/NIMH NIH HHS/ -- R01 MH59199/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Dec 24;462(7276):1065-9. doi: 10.1038/nature08628. Epub 2009 Dec 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/cytology/drug effects/*growth & ; development/*metabolism/ultrastructure ; Female ; Gene Expression Regulation, Developmental ; Male ; Mice ; Mice, Knockout ; Neuropilin-1/metabolism ; Neuropilin-2/metabolism ; Pyramidal Cells/*cytology/drug effects/*growth & development/ultrastructure ; Recombinant Proteins/pharmacology ; Semaphorins/genetics/*metabolism/pharmacology ; Signal Transduction ; Synapses/drug effects/*physiology/ultrastructure
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Notch and EGFR pathway interaction regulates neural stem cell number and self-renewal (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-09-17
    Description: Specialized cellular microenvironments, or 'niches', modulate stem cell properties, including cell number, self-renewal and fate decisions. In the adult brain, niches that maintain a source of neural stem cells (NSCs) and neural progenitor cells (NPCs) are the subventricular zone (SVZ) of the lateral ventricle and the dentate gyrus of the hippocampus. The size of the NSC population of the SVZ at any time is the result of several ongoing processes, including self-renewal, cell differentiation, and cell death. Maintaining the balance between NSCs and NPCs in the SVZ niche is critical to supply the brain with specific neural populations, both under normal conditions or after injury. A fundamental question relevant to both normal development and to cell-based repair strategies in the central nervous system is how the balance of different NSC and NPC populations is maintained in the niche. EGFR (epidermal growth factor receptor) and Notch signalling pathways have fundamental roles during development of multicellular organisms. In Drosophila and in Caenorhabditis elegans these pathways may have either cooperative or antagonistic functions. In the SVZ, Notch regulates NSC identity and self-renewal, whereas EGFR specifically affects NPC proliferation and migration. This suggests that interplay of these two pathways may maintain the balance between NSC and NPC numbers. Here we show that functional cell-cell interaction between NPCs and NSCs through EGFR and Notch signalling has a crucial role in maintaining the balance between these cell populations in the SVZ. Enhanced EGFR signalling in vivo results in the expansion of the NPC pool, and reduces NSC number and self-renewal. This occurs through a non-cell-autonomous mechanism involving EGFR-mediated regulation of Notch signalling. Our findings define a novel interaction between EGFR and Notch pathways in the adult SVZ, and thus provide a mechanism for NSC and NPC pool maintenance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941915/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941915/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aguirre, Adan -- Rubio, Maria E -- Gallo, Vittorio -- K99NS057944/NS/NINDS NIH HHS/ -- P30HD40677/HD/NICHD NIH HHS/ -- R00 NS057944/NS/NINDS NIH HHS/ -- R01 DC006881/DC/NIDCD NIH HHS/ -- R01 DC006881-03/DC/NIDCD NIH HHS/ -- R01 DC006881-04/DC/NIDCD NIH HHS/ -- R01DC006881/DC/NIDCD NIH HHS/ -- R01NS045702/NS/NINDS NIH HHS/ -- R01NS056427/NS/NINDS NIH HHS/ -- R0O NS057944-03/NS/NINDS NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):323-7. doi: 10.1038/nature09347.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuroscience Research, Children's National Medical Center, Washington, District of Columbia 20010, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20844536" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Division ; Humans ; Membrane Proteins/deficiency/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/deficiency/genetics/metabolism ; Neurons/*cytology ; Protein Binding ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Receptor, Notch1/metabolism ; Receptors, Notch/*metabolism ; *Signal Transduction ; Stem Cell Niche/cytology ; Stem Cells/*cytology ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Bergmann glial AMPA receptors are required for fine motor coordination (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-07
    Description: The impact of glial neurotransmitter receptors in vivo is still elusive. In the cerebellum, Bergmann glial (BG) cells express alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPARs) composed exclusively of GluA1 and/or GluA4 subunits. With the use of conditional gene inactivation, we found that the majority of cerebellar GluA1/A4-type AMPARs are expressed in BG cells. In young mice, deletion of BG AMPARs resulted in retraction of glial appendages from Purkinje cell (PC) synapses, increased amplitude and duration of evoked PC currents, and a delayed formation of glutamatergic synapses. In adult mice, AMPAR inactivation also caused retraction of glial processes. The physiological and structural changes were accompanied by behavioral impairments in fine motor coordination. Thus, BG AMPARs are essential to optimize synaptic integration and cerebellar output function throughout life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saab, Aiman S -- Neumeyer, Alexander -- Jahn, Hannah M -- Cupido, Alexander -- Simek, Antonia A M -- Boele, Henk-Jan -- Scheller, Anja -- Le Meur, Karim -- Gotz, Magdalena -- Monyer, Hannah -- Sprengel, Rolf -- Rubio, Maria E -- Deitmer, Joachim W -- De Zeeuw, Chris I -- Kirchhoff, Frank -- R01-DC006881/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):749-53. doi: 10.1126/science.1221140. Epub 2012 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology, University of Saarland, Homburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22767895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism/ultrastructure ; Cerebellar Cortex/*cytology/growth & development/physiology ; Conditioning, Eyelid ; Excitatory Postsynaptic Potentials ; Locomotion ; Mice ; Mice, Knockout ; *Motor Activity ; Neurites/physiology/ultrastructure ; Patch-Clamp Techniques ; Psychomotor Performance ; Purkinje Cells/cytology/physiology ; Receptors, AMPA/*metabolism ; Signal Transduction ; Synapses/physiology/ultrastructure ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Derivation of midbrain dopamine neurons from human embryonic stem cells (2004)
    National Academy of Sciences
    Details
    Publication Date: 2004-08-13
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Magnetic field generation from primordial black hole distributions (2021)
    Oxford University Press
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    Publication Date: 2021-03-13
    Description: We introduce a statistical method for estimating magnetic field fluctuations generated from primordial black hole (PBH) populations. To that end, we consider monochromatic and extended Press-Schechter PBH mass functions, such that each constituent is capable of producing its own magnetic field due to some given physical mechanism. Assuming linear correlation between magnetic field fluctuations and matter over-densities, our estimates depend on the mass function, the physical field generation mechanism by each PBH constituent, and the characteristic PBH separation. After computing the power spectrum of magnetic field fluctuations, we apply our formalism to study the plausibility that two particular field generation mechanisms could have given rise to the expected seed fields according to current observational constraints. The first mechanism is the Biermann battery and the second one is due to the accretion of magnetic monopoles at PBH formation, constituting magnetic PBHs. Our results show that, for monochromatic distributions, it does not seem to be possible to generate sufficiently intense seed fields in any of the two field generation mechanisms. For extended distributions, it is also not possible to generate the required seed field by only assuming a Biermann battery mechanism. In fact, we report an average seed field by this mechanism of about 10−47 G, at z = 20. For the case of magnetic monopoles we instead assume that the seed values from the literature are achieved and calculate the necessary number density of monopoles. In this case we obtain values that are below the upper limits from current constraints.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press on behalf of The Royal Astronomical Society.
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