Interactions of γ-L-glutamyltaurine with excitatory aminoacidergic neurotransmission

Abstract

The in vitro effects of γ-L-glutamyltaurine on different stages of excitatory aminoacidergic neurotransmission were tested with γ-D-glutamyltaurine as reference. γ-L-Glutamyltaurine enhanced the K⁺-stimulated release of [³H]glutamate from cerebral cortical slices (25% at 0.1 mM) and slightly inhibited the uptake by crude brain synaptosomal preparations (about 10% at 1 mM). γ-L-Glutamyltaurine was also a weak displacer of glutamate and its agonists from their binding sites in brain synaptic membrane preparations, being, however, less selective to quisqualate (QA) sites than γ-D-glutamyltaurine. The basal influx of Ca²⁺ into cultured cerebellar granular cells was not affected by 1 mM γ-L-glutamyltaurine, but the glutamate- and its agonist-activated influx was significantly inhibited in low-Mg²⁺ (0.1 mM) and Mg²⁺-free media. The glutamate-evoked increase in free intracellular Ca²⁺ and the kainate-activated formation of cGMP in cerebellar slices were both markedly inhibited by 0.1 mM γ-L-giutamyltaurine. We propose that γ-L-glutamyltaurine may act as endogenous modulator in excitatory aminoacidergic neurotransmission.