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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/11808

Title: Glycine enhances microglial intracellular calcium signaling. A role for sodium-coupled neutral amino acid transporters
Authors: VAN DEN EYNDEN, Jimmy
NOTELAERS, Kristof
BRONE, Bert
JANSSEN, Daniel
NELISSEN, Katherine
SAHEBALI, Sheen
SMOLDERS, Inge
HELLINGS, Niels
STEELS, Paul
RIGO, Jean-Michel
Issue Date: 2011
Citation: PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 461(4), p. 481-491
Abstract: The inhibitory neurotransmitter glycine is known to enhance microglial nitric oxide production. However, up to now, the mechanism is undocumented. Since calcium is an important second messenger in both immune and glial cells, we studied the effects of glycine on intracellular calcium signaling. We found that millimolar concentrations of glycine enhance microglial intracellular calcium transients induced by 100 μMATP or by 500 nMthapsigargin. This modulation was unaffected by the glycine receptor antagonist strychnine and could not be mimicked by glycine receptor agonists such as taurine or β-alanine, indicating glycine receptor independency. The modulation of calcium responses could be mimicked by several structurally related amino acids (e.g., serine, alanine, or glutamine) and was inhibited in the presence of the neutral amino acid transporter substrate α-aminoisobutyric acid (AIB). We correlated these findings to immunofluorescence glycine uptake experiments which showed a clear glycine uptake which was inhibited by AIB. Furthermore, all amino acids that were shown to modulate calcium responses also evoked AIB-sensitive inward currents, mainly carried by sodium, as demonstrated by patch clamp experiments. Based on these findings, we propose that sodium-coupled neutral amino acid transporters are responsible for the observed glycine modulation of intracellular calcium responses.
URI: http://hdl.handle.net/1942/11808
DOI: 10.1007/s00424-011-0939-0
ISI #: 000289234800007
Category: A1
Type: Journal Contribution
Validation: ecoom, 2012
Appears in Collections: Research publications

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