Modulation of Calcium Channels by Taurine Acting Via a Metabotropic-like Glycine Receptor

Taurine is one of the most abundant free amino acids in the central nervous system, where it displays several functions. However, its molecular targets remain unknown. It is well known that taurine can activate GABA-A and strychnine-sensitive glycine receptors, which increases a chloride conductance...

Full description

Saved in:
Bibliographic Details
Published in:Cellular and molecular neurobiology 2010-11, Vol.30 (8), p.1225-1233
Main Authors: Albiñana, E, Sacristán, S, Martín del Río, R, Solís, J. M, Hernández-Guijo, J. M
Format: Article
Language:English
Subjects:
Animals
Biomedical and Life Sciences
Biomedicine
calcium channels
Calcium Channels - metabolism
Cattle
Cell Biology
Chromaffin Cells - drug effects
Chromaffin Cells - metabolism
G-proteins
gamma-Aminobutyric Acid - metabolism
Glycine - pharmacology
Glycine receptors
GTP-Binding Proteins - metabolism
Ion Channel Gating - drug effects
Membrane Glycoproteins - metabolism
Membrane Transport Proteins - metabolism
Neurobiology
Neurosciences
Original Research
Receptors, GABA-B - metabolism
Receptors, Glycine - metabolism
taurine
Taurine - pharmacology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Taurine is one of the most abundant free amino acids in the central nervous system, where it displays several functions. However, its molecular targets remain unknown. It is well known that taurine can activate GABA-A and strychnine-sensitive glycine receptors, which increases a chloride conductance. In this study, we describe that acute application of taurine induces a dose-dependent inhibition of voltage-dependent calcium channels in chromaffin cells from bovine adrenal medullae. This taurine effect was not explained by the activation of either GABA-A, GABA-B or strychnine-sensitive glycine receptors. Interestingly, glycine mimicked the modulatory action exerted by taurine on calcium channels, although the acute application of glycine did not elicit any ionic current in these cells. Additionally, the modulation of calcium channels exerted by both taurine and glycine was prevented by the intracellular dialysis of GDP-β-S. Thus, the modulation of voltage-dependent calcium channels by taurine seems to be mediated by a metabotropic-like glycinergic receptor coupled to G-protein activation in a membrane delimited pathway.
ISSN:0272-4340
1573-6830
1573-6830
DOI:10.1007/s10571-010-9574-0