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Articles, Cellular/Molecular

Progressive Degeneration of Dopaminergic Neurons through TRP Channel-Induced Cell Death

Archana Nagarajan, Ye Ning, Kaja Reisner, Zafir Buraei, Jan Petter Larsen, Oliver Hobert and Maria Doitsidou
Journal of Neuroscience 23 April 2014, 34 (17) 5738-5746; DOI: https://doi.org/10.1523/JNEUROSCI.4540-13.2014
Archana Nagarajan
1Center for Organelle Research, University of Stavanger, 4036 Stavanger, Norway,
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Ye Ning
2Norwegian Center for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway,
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Kaja Reisner
1Center for Organelle Research, University of Stavanger, 4036 Stavanger, Norway,
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Zafir Buraei
3Department of Biology and Health Sciences, Pace University, New York, New York 10038, and
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Jan Petter Larsen
2Norwegian Center for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway,
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Oliver Hobert
4Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University Medical Center, New York, New York 10032
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Maria Doitsidou
1Center for Organelle Research, University of Stavanger, 4036 Stavanger, Norway,
2Norwegian Center for Movement Disorders, Stavanger University Hospital, 4011 Stavanger, Norway,
4Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University Medical Center, New York, New York 10032
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Abstract

Progressive neurodegenerative diseases are among the most frequently occurring aging-associated human pathologies. In a screen for Caenorhabditis elegans mutant animals that lack their normal complement of dopaminergic neurons, we identified two strains with progressive loss of dopaminergic neurons during postembryonic life. Through whole-genome sequencing we show that both strains harbor dominant (d), gain-of-function mutations in the Transient Receptor Potential (TRP) mechanosensory channel trp-4, a member of the invertebrate and vertebrate TRPN-type of the TRP family channels. Gain-of-function mutations in TRP channels have not been previously implicated in dopaminergic neuronal degeneration. We show that trp-4(d) induces cell death in dopamine neurons through a defined, calcium-related downstream pathway.

  • C. elegans
  • calcium
  • cell death
  • dopaminergic neurons
  • neurodegeneration
  • TRP channels
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The Journal of Neuroscience: 34 (17)
Journal of Neuroscience
Vol. 34, Issue 17
23 Apr 2014
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Progressive Degeneration of Dopaminergic Neurons through TRP Channel-Induced Cell Death
Archana Nagarajan, Ye Ning, Kaja Reisner, Zafir Buraei, Jan Petter Larsen, Oliver Hobert, Maria Doitsidou
Journal of Neuroscience 23 April 2014, 34 (17) 5738-5746; DOI: 10.1523/JNEUROSCI.4540-13.2014

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Progressive Degeneration of Dopaminergic Neurons through TRP Channel-Induced Cell Death
Archana Nagarajan, Ye Ning, Kaja Reisner, Zafir Buraei, Jan Petter Larsen, Oliver Hobert, Maria Doitsidou
Journal of Neuroscience 23 April 2014, 34 (17) 5738-5746; DOI: 10.1523/JNEUROSCI.4540-13.2014
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Keywords

  • C. elegans
  • calcium
  • cell death
  • dopaminergic neurons
  • neurodegeneration
  • TRP channels

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  • An overactivation of mGluRs via TRP channels produces necrotic death in DAergic neurons
    Nicola B Mercuri
    Published on: 26 September 2014
  • Published on: (26 September 2014)
    Page navigation anchor for An overactivation of mGluRs via TRP channels produces necrotic death in DAergic neurons
    An overactivation of mGluRs via TRP channels produces necrotic death in DAergic neurons
    • Nicola B Mercuri, Professor of Neurology

    The work of Nagarajan et al. (2014) on C. elegans mutants shows that subunits of a transient receptor potential (TRP) channel allow calcium to enter the cell, thus leading to necrotic-like death of dopaminergic neurons. We believe that the toxic action of beta-N -Methylamino alanine (BMAA) in dopaminergic neurons of rodents (Cucchiaroni et al., 2010) could recapitulate some features of cell death described in the worm....

    Show More

    The work of Nagarajan et al. (2014) on C. elegans mutants shows that subunits of a transient receptor potential (TRP) channel allow calcium to enter the cell, thus leading to necrotic-like death of dopaminergic neurons. We believe that the toxic action of beta-N -Methylamino alanine (BMAA) in dopaminergic neurons of rodents (Cucchiaroni et al., 2010) could recapitulate some features of cell death described in the worm. This brings into the arena the attractive hypothesis that not only a mutation but also unphysiological stimulation of TRP channels by neurotransmitters, drugs, and toxins could lead to degeneration of the dopaminergic system.

    Reference

    Cucchiaroni et al.,. Metabotropic glutamate receptor 1 mediates the electrophysiological and toxic actions of the cycad derivative beta-N- Methylamino-L-alanine on substantia nigra pars compacta DAergic neurons. J Neurosci. 2010 Apr 14;30(15):5176-88.

    Conflict of Interest:

    None declared

    Show Less
    Competing Interests: None declared.

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