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5-HT2A receptor-mediated outward current in C6 glioma cells is mimicked by intracellular IP3 release

J T Bartrup1, N R Newberry

  • 1Oxford University-SmithKline Beecham Centre for Applied Neuropsychobiology, University Department of Clinical Pharmacology, Radcliffe Infirmary, UK.

Neuroreport
|June 2, 1994
PubMed

Insights

The C6 glioma cell line

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • C6 glioma cells express serotonin 5-HT2A receptors.
  • Activation of these receptors is known to elevate intracellular calcium.
  • Understanding the downstream signaling is crucial for neurological research.

Purpose of the Study:

  • To investigate the electrophysiological effects of 5-hydroxytryptamine (5-HT) on C6 glioma cells.
  • To elucidate the signaling pathway downstream of 5-HT2A receptor activation in this cell line.

Main Methods:

  • Whole-cell voltage-clamp recordings were performed on C6 glioma cells.
  • Cells were exposed to 5-HT, and responses were measured.
  • Pharmacological blockers (ketanserin, spiperone) and EGTA were used to probe the mechanism.
  • Inositol (1,4,5) trisphosphate (IP3) was released intracellularly using caged compounds to mimic the response.

Main Results:

  • 5-HT induced an outward current in C6 glioma cells.
  • This current was inhibited by 5-HT2A receptor antagonists and intracellular calcium chelation (EGTA).
  • Intracellular IP3 release mimicked the 5-HT-induced current, with similar reversal potentials.
  • These findings suggest a signaling cascade involving IP3 production and calcium release.

Conclusions:

  • 5-HT activates 5-HT2A receptors in C6 glioma cells, leading to IP3 production.
  • Increased intracellular calcium triggers the opening of calcium-activated potassium channels, causing an outward current.
  • This study clarifies the signaling pathway for 5-HT2A receptor activation in C6 glioma cells.

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