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      Differential Regulation of AMPA Receptor and GABA Receptor Trafficking by Tumor Necrosis Factor-α

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          Abstract

          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 of normal surface expression of AMPA receptors. Here we demonstrate that TNFα acts on neuronal TNFR1 receptors to preferentially exocytose glutamate receptor 2-lacking AMPA receptors through a phosphatidylinositol 3 kinase-dependent process. This increases excitatory synaptic strength while changing the molecular stoichiometry of synaptic AMPA receptors. Conversely, TNFα causes an endocytosis of GABA A receptors, resulting in fewer surface GABA A receptors and a decrease in inhibitory synaptic strength. These results suggest that TNFα can regulate neuronal circuit homeostasis in a manner that may exacerbate excitotoxic damage resulting from neuronal insults.

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          Author and article information

          Journal
          J Neurosci
          J. Neurosci
          jneuro
          The Journal of Neuroscience
          Society for Neuroscience
          0270-6474
          1529-2401
          23 March 2005
          : 25
          : 12
          : 3219-3228
          Affiliations
          [1 ]Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford Medical School, Palo Alto, California 94305, and [2 ]California Pacific Medical Research Institute, San Francisco, California 94115
          Article
          PMC6725093 PMC6725093 6725093 00253219
          10.1523/JNEUROSCI.4486-04.2005
          6725093
          15788779
          fc0294f6-8f6d-49b4-b1f8-8ac05eba90ff
          Copyright © 2005 Society for Neuroscience 0270-6474/05/253219-10.00/0
          History
          : 17 February 2005
          : 1 November 2004
          : 10 January 2005
          Categories
          Cellular/Molecular
          Custom metadata
          3219
          ARTICLE

          cytokine,trafficking,glutamate,synaptic,receptor,GABA
          cytokine, trafficking, glutamate, synaptic, receptor, GABA

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