J Physiol Volume 559, Number 1, 35-40, August 15, 2004 DOI: 10.1113/jphysiol.2004.070763
A novel physiological mechanism of glycine-induced immunomodulation: Na+-coupled amino acid transporter currents in cultured brain macrophages
Tom Schilling and
Claudia Eder
Institute of Physiology, Humboldt University, Tucholsky Str. 2, D-10117 Berlin, Germany
Glycine is known to modulate immune cell responses. However, the physiological mechanisms underlying inhibitory effects of glycine on macrophages are not well understood. Here we show that glycine is capable of inducing inward currents in brain macrophages (microglia). In contrast to glycine, the glycine receptor agonist taurine failed to elicit currents. Glycine-evoked currents of brain macrophages were unaffected by strychnine, Cl–-free extracellular solution, N-[3-(4'-fluorophenyl)-3-(4'-phenylphenoxy)propyl])sarcosine (NFPS) and amoxapine, but were abolished upon omission of extracellular Na+. Furthermore, glycine caused increases in the intracellular Na+ concentration and pronounced membrane depolarization. Glycine-evoked depolarization was Na+ dependent and occurred independently of the intracellular Cl– concentration. Similarly to glycine, glutamine and 
-(methylamino)isobutyric acid (MeAIB) elicited inward currents in brain macrophages. In the presence of either glutamine or MeAIB, glycine-induced currents were inhibited. It is concluded that neither functional glycine receptors nor glycine transporters are expressed in brain macrophages. We suggest that glycine mediates its effects by activation of system A Na+-coupled neutral amino acid transporters.
(Received 28 June 2004;
accepted after revision 7 July 2004;
first published online 8 July 2004)
Corresponding author C. Eder: Institute of Physiology, Humboldt University, Tucholsky Str. 2, D-10117 Berlin, Germany. Email: claudia.eder{at}charite.de
Copyright © 2004 The Physiological Society.
