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Selective interference with TRPC3/6 channels disrupts OX1 receptor signalling via NCX and reveals a distinct calcium

Lauri M Louhivuori1, Linda Jansson, Tommy Nordström

  • 1Biomedicum Helsinki, Institute of Biomedicine/Physiology, University of Helsinki, Finland.

Cell Calcium
|August 24, 2010
PubMed

Insights

Transient Receptor Potential Canonical (TRPC) channels are crucial for neuronal development. This study reveals that sodium entry via TRPC3/6 channels mediates calcium influx in some neurons, while other pathways exist in different neuronal subpopulations.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Ion Channel Physiology

Background:

  • Transient Receptor Potential Canonical (TRPC) channels are implicated in neuronal plasticity and development.
  • Calcium (Ca2+) influx is a key mechanism underlying the trophic actions of TRPC channels.

Purpose of the Study:

  • To investigate the role of sodium (Na+) entry in receptor-mediated calcium influx through TRPC channels in a neuronal cell model.
  • To differentiate between distinct mechanisms of calcium entry in neuronal subpopulations.

Main Methods:

  • Utilized differentiated human IMR32 neuroblastoma cells as a neuronal model.
  • Stimulated orexin/hypocretin and bradykinin receptors to induce calcium influx.
  • Assessed the impact of protein kinase C activation, Na+/Ca2+ exchanger inhibitors, and TRPC3/6 channel disruption on calcium entry.
  • Investigated the effect of polyvalent cations (ruthenium red, spermine, Gd3+) on calcium influx.

Main Results:

  • Identified a subpopulation of neurons where Na+ entry via TRPC3/6 channels is central to receptor-mediated calcium influx.
  • Demonstrated that this Na+-dependent Ca2+ influx is inhibited by protein kinase C, Na+/Ca2+ exchanger inhibitors, and TRPC3/6 channel disruption.
  • Observed a distinct subpopulation of neurons exhibiting Na+-independent Ca2+ entry, sensitive to polyvalent cations but unaffected by the aforementioned treatments.
  • Suggested a functional interaction between the Na+/Ca2+ exchanger (NCX) and TRPC channels in mediating receptor-activated calcium influx.

Conclusions:

  • Receptor-mediated calcium influx in neuronal cells involves at least two distinct pathways.
  • Sodium entry through TRPC3/6 channels, potentially coupled with the Na+/Ca2+ exchanger, plays a significant role in a subset of neurons.
  • Understanding these distinct calcium influx mechanisms is vital for comprehending neuronal plasticity and development.

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