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    • Ben Anthony Barres: Influence Statistics

      Ben Anthony Barres

      Ben Anthony Barres

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      Department of Neurobiology, Stanford University School of Medicine, 94305-5125, Stanford, CA, USA | Department of Neurobiology, Stanford University, Palo Alto, CA | Department ...

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      Ben Anthony Barres:Expert Impact

      Concepts for whichBen Anthony Barreshas direct influence:Schwann cells,Oligodendrocyte differentiation,Astrocyte activation,Synapse formation,Cns myelination,Endothelial cells,Retinal ganglion cells,Central nervous.

      Ben Anthony Barres:KOL impact

      Concepts related to the work of other authors for whichfor which Ben Anthony Barres has influence:Central nervous,Multiple sclerosis,Spinal cord,Gene expression,Glial cells,Alzheimer disease,White matter.

      KOL Resume for Ben Anthony Barres

      Year
      2022

      Department of Neurobiology, Stanford University School of Medicine, 94305-5125, Stanford, CA, USA

      2021

      Department of Neurobiology, Stanford University, Palo Alto, CA

      2020

      Department of Neurobiology, School of Medicine, Stanford University, 94305, Stanford, CA, USA

      2019

      Stanford University School of Medicine, Department of Neurobiology, Stanford, CA 94305, USA

      2018

      Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA

      2017

      Department of Neurobiology, School of Medicine, Stanford University, 94305, Stanford, California, USA

      2016

      Department of Neurobiology, Stanford University School of Medicine, Palo Alto, California 94305, USA.

      2015

      Neurobiology, and

      2014

      Department of Neurobiology, Stanford University, Stanford, CA 94110, USA

      Stanford University School of Medicine, Stanford, California 94305

      2013

      Stanford University School of Medicine, Departments of Neurobiology and

      2012

      Department of Neurobiology, Stanford University School of Medicine, D231 Fairchild Building, 299 Campus Drive, Stanford, CA 94305, USA

      2011

      Department of Neurobiology, Stanford School of Medicine, Stanford, CA 94305, USA

      Neurobiology, Stanford University School of Medicine, Stanford, California, 94305,

      2010

      Department of Neurobiology, Stanford University Medical Center, Fairchild Building D-200, 94305, Stanford, California, USA

      Neurobiology, Stanford University School of Medicine, Stanford University, Stanford, CA 94305

      2009

      Department of Neurobiology, and

      Stanford University School of Medicine, Stanford, CA, USA

      2008

      Department of Neurobiology, Fairchild Science Building D235, Stanford University School of Medicine, Palo Alto, CA 94305, USA

      Developmental Biology,

      2007

      Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305; email: ,

      2006

      Department of Neurobiology, Stanford University School ofMedicine, 299 Campus Drive, Fairchild Building Room D235, 94305-5125, Stanford, CA, USA

      2005

      Stanford University School of Medicine, Neurobiology Department, Sherman Fairchild Science Building, Room D129, 299 Campus Drive, Stanford, California 94305-5125, USA.

      2004

      Department of Neurobiology, Stanford University School of Medicine, Stanford, California

      2003

      Department of Neurobiology, Stanford University, Fairchild Building, 299 Campus Drive, Stanford, CA 94305 USA

      2002

      Department of Neurobiology, Stanford University School of Medicine, 94305-5125, Stanford, California, USA

      2001

      Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305 USA

      2000

      Department of Neurobiology, Stanford University School of Medicine, Fairchild Science Building, 94305, Stanford, California, USA

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      Sample of concepts for which Ben Anthony Barres is among the top experts in the world.
      Concept World rank
      mir219 myelination #1
      glialneuronal signals significance #1
      lm22a4 survival #1
      intracellular timer #1
      synaptic activity glia #1
      mice mice astrocytes #1
      clear myelin #1
      continued study keys #1
      interleukin33 astrocytes #1
      astrocyte nerve fibers #1
      opposite effects myelination #1
      primary opcs iopcs #1
      microtubules primary #1
      receptivity synaptic #1
      activity camp elevation #1
      dawley synapses toxins #1
      synapses new findings #1
      mrf transcriptional regulator #1
      chromatin remodeling molecules #1
      actin disassembly proteins #1
      infiltration immunological response #1
      axons insights #1
      gbm cell types #1
      mertk pns injury #1
      cellular user manual #1
      epileptic tumor foci #1
      12weekold wild type #1
      astrocytesecreted proteins hevin #1
      periphery cns synapses #1
      sulfatide rgc axons #1
      cellautonomous regulation #1
      gbp undercut animals #1
      p57kip2 levels time #1
      antisense oligodeoxynucleotides inactivation #1
      result nonneuronal cells #1
      microglial origins #1
      trhrdsgcs #1
      tsp4 antagonists #1
      myelination oligodendrocyte development #1
      synaptogenesis vitro #1
      regulators synaptic connectivity #1
      data detailed dissection #1
      c1q hippocampal circuitry #1
      cns projection neurons #1
      maturation mice models #1
      glia passive bystanders #1
      microglia wlodarczyk #1
      camp cultured rgcs #1
      pns highlights features #1
      multielectrode silicon chip #1
      Sign-in to see all concepts, it's free!

      Prominent publications by Ben Anthony Barres

      KOL-Index: 16707

      Glia constitute 90% of cells in the human nervous system, but relatively little is known about their functions. We have been focusing on the potential synaptic roles of glia in the CNS. We recently found that astrocytes increase the number of mature, functional synapses on retinal ganglion cells (RGCs) by sevenfold and are required for synaptic maintenance in vitro. These observations raised the question of whether glia similarly enhance synapse formation by other neuron types. Here we ...

      Known for Schwann Cells | Synapse Formation | Spinal Motor Neurons | Astrocytes Cell | Culture Media
      KOL-Index: 13108

      Ineffective myelin debris clearance is a major factor contributing to the poor regenerative ability of the central nervous system. In stark contrast, rapid clearance of myelin debris from the injured peripheral nervous system (PNS) is one of the keys to this system's remarkable regenerative capacity, but the molecular mechanisms driving PNS myelin clearance are incompletely understood. We set out to discover new pathways of PNS myelin clearance to identify novel strategies for activating ...

      Known for Nerve Injury | Schwann Cells | Mouse Model | Myelin Debris | Central Nervous
      KOL-Index: 12417

      In the developing central nervous system (CNS), the control of synapse number and function is critical to the formation of neural circuits. We previously demonstrated that astrocyte-secreted factors powerfully induce the formation of functional excitatory synapses between CNS neurons. Astrocyte-secreted thrombospondins induce the formation of structural synapses, but these synapses are postsynaptically silent. Here we use biochemical fractionation of astrocyte-conditioned medium to ...

      Known for Excitatory Synapses | Ampa Receptors | Hippocampus Humans | Male Mice Mice | Cns Neurons
      KOL-Index: 12356

      NMDA excitotoxicity has been proposed to mediate the death of retinal ganglion cells (RGCs) in glaucoma and ischemia. Here, we reexamine the effects of glutamate and NMDA on rat RGCs in vitro and in situ. We show that highly purified RGCs express NR1 and NR2 receptor subunits by Western blotting and immunostaining, and functional NMDA receptor channels by whole-cell patch-clamp recording. Nevertheless, high concentrations of glutamate or NMDA failed to induce the death of purified RGCs, ...

      Known for Retinal Ganglion Cells | Nmda Excitotoxicity | Rat Rgcs | Western Blotting | Cell Death
      KOL-Index: 11911

      Opioid pain medications have detrimental side effects including analgesic tolerance and opioid-induced hyperalgesia (OIH). Tolerance and OIH counteract opioid analgesia and drive dose escalation. The cell types and receptors on which opioids act to initiate these maladaptive processes remain disputed, which has prevented the development of therapies to maximize and sustain opioid analgesic efficacy. We found that μ opioid receptors (MORs) expressed by primary afferent nociceptors ...

      Known for Morphine Tolerance | Analgesic Efficacy | Spinal Microglia | Opioid Receptors | Nociceptors Pain
      KOL-Index: 11811

      The timing of oligodendrocyte differentiation is thought to depend on an intrinsic clock in oligodendrocyte precursor cells that counts time or cell divisions and limits precursor cell proliferation. We show here that this clock mechanism can be separated into a counting component and an effector component that stops cell proliferation: whereas the counting mechanism is driven by mitogens that activate cell-surface receptors, the effector mechanism depends on hydrophobic signals that ...

      Known for Retinoic Acid | Thyroid Hormone | Oligodendrocyte Development | Precursor Cells | Timing Differentiation
      KOL-Index: 11649

      In the mammalian CNS, glial cells repel axons during development and inhibit axon regeneration after injury. It is unknown whether the same repulsive axon guidance molecules expressed by glia and their precursors during development also play a role in inhibiting regeneration in the injured CNS. Here we investigate whether optic nerve glial cells express semaphorin family members and, if so, whether these semaphorins inhibit axon growth by retinal ganglion cells (RGCs). We show that each ...

      Known for Axon Growth | Retinal Ganglion Cells | Nerve Regeneration | Injured Cns | Semaphorins Sema5a
      KOL-Index: 11619

      To investigate the role of microRNAs in regulating oligodendrocyte (OL) differentiation and myelination, we utilized transgenic mice in which microRNA processing was disrupted in OL precursor cells (OPCs) and OLs by targeted deletion of Dicer1. We found that inhibition of OPC-OL miRNA processing disrupts normal CNS myelination and that OPCs lacking mature miRNAs fail to differentiate normally in vitro. We identified three miRNAs (miR-219, miR-138, and miR-338) that are induced 10-100x ...

      Known for Myelin Proteins | Transcription Factors | Oligodendrocyte Differentiation | Transgenic Micrornas | Spraguedawley Receptor
      KOL-Index: 11521

      Here we have investigated the mechanisms that control astrocyte differentiation within the developing rat optic nerve. Astrocytes are normally generated by astrocyte precursor cells within the embryonic optic nerve. We show that there is a close temporal and spatial correlation between endothelial and astrocyte differentiation. We tested the potential role of endothelial cells in inducing astrocyte differentiation by developing an immunopanning method to highly purify endothelial cells ...

      Known for Astrocyte Differentiation | Endothelial Cells | Inhibitory Factor Lif | Messenger Rats | Optic Nerve
      KOL-Index: 11467

      Understanding the cell-cell interactions that control CNS development and function has long been limited by the lack of methods to cleanly separate neural cell types. Here we describe methods for the prospective isolation and purification of astrocytes, neurons, and oligodendrocytes from developing and mature mouse forebrain. We used FACS (fluorescent-activated cell sorting) to isolate astrocytes from transgenic mice that express enhanced green fluorescent protein (EGFP) under the ...

      Known for Astrocytes Neurons | Transcriptome Database | Brain Development | Transgenic Mice | Astrocyte Expression
      KOL-Index: 11308

      Astrocytes regulate synaptic connectivity in the CNS through secreted signals. Here we identified two astrocyte-secreted proteins, hevin and SPARC, as regulators of excitatory synaptogenesis in vitro and in vivo. Hevin induces the formation of synapses between cultured rat retinal ganglion cells. SPARC is not synaptogenic, but specifically antagonizes synaptogenic function of hevin. Hevin and SPARC are expressed by astrocytes in the superior colliculus, the synaptic target of retinal ...

      Known for Hevin Sparc | Secreted Proteins | Excitatory Synaptogenesis | Formation Synapses | Synaptic Connectivity
      KOL-Index: 11083

      The specific function of microglia, the tissue resident macrophages of the brain and spinal cord, has been difficult to ascertain because of a lack of tools to distinguish microglia from other immune cells, thereby limiting specific immunostaining, purification, and manipulation. Because of their unique developmental origins and predicted functions, the distinction of microglia from other myeloid cells is critically important for understanding brain development and disease; better tools ...

      Known for Human Cns | New Tools | Microglia Mouse | Specific Function | Brain Development
      KOL-Index: 10883

      Synapse loss in Alzheimer's disease (AD) correlates with cognitive decline. Involvement of microglia and complement in AD has been attributed to neuroinflammation, prominent late in disease. Here we show in mouse models that complement and microglia mediate synaptic loss early in AD. C1q, the initiating protein of the classical complement cascade, is increased and associated with synapses before overt plaque deposition. Inhibition of C1q, C3, or the microglial complement receptor CR3 ...

      Known for Synapse Loss | Complement Microglia | Mouse Models | Mediate Early | Disease Amyloid
      KOL-Index: 10862

      Here, we describe a novel mechanism for the rapid regulation of surface levels of the neurotrophin receptor TrkB. Unlike nodose ganglion neurons, both retinal ganglion cells (RGCs) and spinal motor neurons (SMNs) in culture display only low levels of surface TrkB, though high levels are present intracellularly. Within minutes of depolarization or cAMP elevation, surface TrkB levels increase by nearly 4-fold, and this increase is not blocked by cycloheximide. These findings suggest that ...

      Known for Plasma Membrane | Cns Neurons | Camp Elevation | Surface Trkb | Peripheral Nervous
      KOL-Index: 10848

      The signaling interactions that control oligodendrocyte generation from their precursor cells have been studied intensively. Much less is known about how astrocyte generation is normally controlled. Here we report the purification and characterization of astrocyte precursor cells (APCs) from the developing rat optic nerve. APCs are antigenically distinct from astrocytes. Both cell types are Pax2(+) and vimentin+, whereas astrocytes are GFAP+ and S100beta+, and the precursor cells are ...

      Known for Precursor Cells | Optic Nerve | Developing Rat | Growth Factor | Apcs Astrocytes

      Key People For Schwann Cells

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      Department of Neurobiology, Stanford University School of Medicine, 94305-5125, Stanford, CA, USA | Department of Neurobiology, Stanford University, Palo Alto, CA | Department of Neurobiology, Stanford University, Stanford, CA, USA | Department of Ne

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