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Glutamate activates NF-kappa B through calpain in neurons

Academic Article
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Overview

authors

  • Scholzke, M. N.
  • Potrovita, I.
  • Subramaniam, Srinivasa
  • Prinz, S.
  • Schwaninger, M.

publication date

  • December 2003

journal

  • European Journal of Neuroscience  Journal

abstract

  • Glutamate induces gene transcription in numerous physiological and pathological conditions. Among the glutamate-responsive transcription factors, NF-kappaB has been mainly implicated in neuronal survival and death. Recent data also suggest a role of NF-kappaB in neural development and memory formation. In non-neuronal cells, degradation of the inhibitor IkappaBalpha represents a key step in NF-kappaB activation. However, little is known of how glutamate activates NF-kappaB in neurons. To investigate the signalling cascade involved we used primary murine cerebellar granule cells. Glutamate induced a rapid reduction of IkappaBalpha levels and nuclear translocation of the NF-kappaB subunit p65. The glutamate-induced reduction of IkappaBalpha levels was blocked by the N-methyl-d-aspartate inhibitor MK801. Specific inhibitors of the proteasome, caspase 3, and the phosphoinositide 3-kinase had no effect on glutamate-induced IkappaBalpha degradation. However, inhibition of the glutamate-activated Ca2+-dependent protease calpain by calpeptin completely blocked IkappaBalpha degradation and reduced the nuclear translocation of p65. Calpeptin also partially blocked glutamate-induced cell death. Our data indicate that the Ca2+-dependent protease calpain is involved in the NF-kappaB activation in neurons in response to N-methyl-d-aspartate receptor occupancy by glutamate. NF-kappaB activation by calpain may mediate the long-term effects of glutamate on neuron survival or memory formation.

subject areas

  • Active Transport, Cell Nucleus
  • Animals
  • Animals, Newborn
  • Calpain
  • Cell Death
  • Cell Differentiation
  • Cell Survival
  • Cells, Cultured
  • Cerebellar Cortex
  • Dipeptides
  • Down-Regulation
  • Enzyme Inhibitors
  • Excitatory Amino Acid Antagonists
  • Glutamic Acid
  • I-kappa B Proteins
  • Immunohistochemistry
  • Memory
  • Mice
  • NF-kappa B
  • Nervous System
  • Neurons
  • Protein Subunits
  • Receptors, N-Methyl-D-Aspartate
  • Signal Transduction
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Research

keywords

  • N-methyl-D-aspartate
  • calcium
  • gene transcription
  • mouse
  • neuron
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Identity

International Standard Serial Number (ISSN)

  • 0953-816X

Digital Object Identifier (DOI)

  • 10.1046/j.1460-9568.2003.03079.x

PubMed ID

  • 14686903
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Additional Document Info

start page

  • 3305

end page

  • 3310

volume

  • 18

issue

  • 12

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