Helmut W Kessels

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Synaptic AMPA receptor plasticity and behavior
    Helmut W Kessels
    Department of Neuroscience, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0634, USA
    Neuron 61:340-50. 2009
  2. pmc Metabotropic NMDA receptor function is required for β-amyloid-induced synaptic depression
    Helmut W Kessels
    Center for Neural Circuits and Behavior, Department of Neuroscience, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 110:4033-8. 2013
  3. pmc Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression
    Sadegh Nabavi
    Center for Neural Circuits and Behavior, Division of Biology, Department of Neuroscience and Section of Neurobiology, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 110:4027-32. 2013
  4. pmc The prion protein as a receptor for amyloid-beta
    Helmut W Kessels
    Center for Neural Circuits and Behavior, 9500 Gilman Drive 0634, University of California at San Diego, La Jolla, California 92093, USA
    Nature 466:E3-4; discussion E4-5. 2010
  5. ncbi request reprint Synapto-depressive effects of amyloid beta require PICK1
    Stephanie Alfonso
    Center for Neural Circuits and Behavior, Departments of Neuroscience and Biology, University of California at San Diego, La Jolla, CA, 92093, USA
    Eur J Neurosci 39:1225-33. 2014

Collaborators

  • Roberto Malinow
  • Richard Huganir
  • Stephanie Alfonso
  • Sadegh Nabavi
  • Charles C Banos
  • Kevin M Guckian
  • Anthone W Dunah
  • Gnanasambandam Kumaravel
  • Edward T Lin
  • Kenneth J Rhodes
  • Timothy R Chan
  • Robert H Scannevin
  • Rocky Fox
  • Jonathan Aow

Detail Information

Publications5

  1. ncbi request reprint Synaptic AMPA receptor plasticity and behavior
    Helmut W Kessels
    Department of Neuroscience, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0634, USA
    Neuron 61:340-50. 2009
    ..We argue that monitoring and manipulating synaptic AMPAR trafficking represents an attractive means to study cognitive function and dysfunction in animal models...
  2. pmc Metabotropic NMDA receptor function is required for β-amyloid-induced synaptic depression
    Helmut W Kessels
    Center for Neural Circuits and Behavior, Department of Neuroscience, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 110:4033-8. 2013
    ..This Aβ-induced signaling mediated by alterations in GluN2B conformation may be a target for therapeutic intervention of Alzheimer's disease...
  3. pmc Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression
    Sadegh Nabavi
    Center for Neural Circuits and Behavior, Division of Biology, Department of Neuroscience and Section of Neurobiology, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 110:4027-32. 2013
    ..Our findings indicate that metabotropic actions of NMDARs can weaken active synapses without raising postsynaptic calcium, thereby revising and expanding the mechanisms controlling synaptic plasticity...
  4. pmc The prion protein as a receptor for amyloid-beta
    Helmut W Kessels
    Center for Neural Circuits and Behavior, 9500 Gilman Drive 0634, University of California at San Diego, La Jolla, California 92093, USA
    Nature 466:E3-4; discussion E4-5. 2010
    ..Here we show that PrP(C) is not required for amyloid-beta-induced synaptic depression, reduction in spine density, or blockade of LTP; our results indicate that amyloid-beta-mediated synaptic defects do not require PrP(c)...
  5. ncbi request reprint Synapto-depressive effects of amyloid beta require PICK1
    Stephanie Alfonso
    Center for Neural Circuits and Behavior, Departments of Neuroscience and Biology, University of California at San Diego, La Jolla, CA, 92093, USA
    Eur J Neurosci 39:1225-33. 2014
    ..We concluded that GluA2-PICK1 interactions are a key component of the effects of Aβ on synapses. ..