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Evidence that TRPC1 is involved in hippocampal glutamate-induced cell death

Academic Article
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Overview

authors

  • Narayanan, K. L.
  • Irmady, K.
  • Subramaniam, Srinivasa
  • Unsicker, K.
  • von Bohlen und Halbach, O.

publication date

  • December 2008

journal

  • Neuroscience Letters  Journal

abstract

  • Massive neuronal activation by glutamate can result in an excessive rise in cytoplasmic calcium, a process ultimately leading to neuronal death. We have investigated the role of the transient receptor potential channel 1 (TRPC1) in mediating glutamate-induced neuron death. We show that 2-APB (a blocker of store-operated Ca2+ entry) dramatically reduces glutamate-induced cell death in hippocampal organotypic slice cultures and that glutamate-induced toxicity is accompanied by an increase in TRPC1 expression. RNAi mediated knock-down ofTRPC1 in slice cultures prevented glutamate-induced cell death, indicating that TRPC1 plays a prominent role in calcium entry following exposure to glutamate. Thus, TRPC1 may represent a promising target for pharmacological interventions to prevent or reduce glutamate-induced neuronal damage.

subject areas

  • Animals
  • Animals, Newborn
  • Atrophy
  • Boron Compounds
  • Calcium
  • Calcium Signaling
  • Cell Death
  • Down-Regulation
  • Glutamic Acid
  • Hippocampus
  • Mice
  • Mice, Inbred C57BL
  • Nerve Degeneration
  • Neurodegenerative Diseases
  • Neurons
  • Neurotoxins
  • Organ Culture Techniques
  • RNA Interference
  • TRPC Cation Channels
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Research

keywords

  • Cell death
  • Glutamate toxicity
  • Mouse
  • RNAi
  • Slice culture
  • TRPC
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Identity

International Standard Serial Number (ISSN)

  • 0304-3940

Digital Object Identifier (DOI)

  • 10.1016/j.neulet.2008.09.034

PubMed ID

  • 18822346
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Additional Document Info

start page

  • 117

end page

  • 122

volume

  • 446

issue

  • 2-3

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