Robert C. Malenka

ORCID: 0000-0002-5428-5211
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neural dynamics and brain function
  • Neurotransmitter Receptor Influence on Behavior
  • Memory and Neural Mechanisms
  • Receptor Mechanisms and Signaling
  • Photoreceptor and optogenetics research
  • Ion channel regulation and function
  • Cellular transport and secretion
  • Neuroscience and Neural Engineering
  • Retinal Development and Disorders
  • Lipid Membrane Structure and Behavior
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neuroendocrine regulation and behavior
  • Psychedelics and Drug Studies
  • Mitochondrial Function and Pathology
  • Cannabis and Cannabinoid Research
  • Genetics and Neurodevelopmental Disorders
  • Neurological disorders and treatments
  • Sleep and Wakefulness Research
  • Nicotinic Acetylcholine Receptors Study
  • Functional Brain Connectivity Studies
  • Neurobiology and Insect Physiology Research
  • Autism Spectrum Disorder Research
  • Tryptophan and brain disorders

Stanford University
2016-2025

Palo Alto University
1982-2014

Howard Hughes Medical Institute
1998-2011

University of California, San Francisco
1993-2008

Stanford Medicine
2007

Cleveland Clinic
2006

Johns Hopkins Medicine
2006

University of California, Davis
2006

Louis Stokes Cleveland VA Medical Center
2006

Johns Hopkins University
2006

Activity-dependent modulation of synaptic efficacy in the brain contributes to neural circuit development and experience-dependent plasticity. Although glia are affected by activity ensheathe synapses, their influence on strength has largely been ignored. Here, we show that a protein produced glia, tumor necrosis factor α (TNFα), enhances increasing surface expression AMPA receptors. Preventing actions endogenous TNFα opposite effects. Thus, continual presence is required for preservation at...

10.1126/science.1067859 article EN Science 2002-03-22

Long-term potentiation and long-term depression (LTP/LTD) can be elicited by activating N-methyl-d-aspartate (NMDA)-type glutamate receptors, typically the coincident activity of pre- postsynaptic neurons. The early phases expression are mediated a redistribution AMPA-type receptors: More receptors added to potentiate synapse or removed weaken synapses. With time, structural changes become apparent, which in general require synthesis new proteins. investigation molecular cellular mechanisms...

10.1101/cshperspect.a005710 article EN Cold Spring Harbor Perspectives in Biology 2012-04-17

The proinflammatory cytokine tumor necrosis factor-α (TNFα) causes a rapid exocytosis of AMPA receptors in hippocampal pyramidal cells and is constitutively required for the maintenance normal surface expression receptors. Here we demonstrate that TNFα acts on neuronal TNFR1 to preferentially exocytose glutamate receptor 2-lacking through phosphatidylinositol 3 kinase-dependent process. This increases excitatory synaptic strength while changing molecular stoichiometry Conversely, an...

10.1523/jneurosci.4486-04.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-03-23
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