Taurine activates glycine and γ-aminobutyric acid A receptors in rat substantia gelatinosa neurons

Abstract

Taurine has been suggested to modulate nociceptive information at the spinal cord level. In this study, the pharmacological properties of taurine were investigated in adult rat substantia gelatinosa (SG) neurons using whole-cell patch-clamp method. We found that taurine seemed to have higher efficacy than glycine on glycine receptors in SG neurons. An increase in chloride conductance was responsible for taurine-induced currents. Taurine at 0.3 mM activated glycine receptors, whereas at 3 mM activated both glycine and gamma-aminobutyric acid A receptors. The currents activated by coapplication of taurine and glycine are cross inhibitive. Altogether these results show that taurine might represent another important neurotransmitter or modulator in SG neurons, which may be involved in antinociception.

The Effect of Subacute Supplementation of Taurine on Spatial Learning and Memory

“…The roles of endogenous taurine in the liver and heart are to increase bile acid secretion by forming bile acid conjugate [2] and regulate Ca 2+ kinetics to protect and improve the heart function [17], respectively. In the brain, taurine is also abundant, especially in the hippocampus, and modulates synaptic transmission as an inhibitory neuromodulator interacting with g-aminobutyric acid type A (GABA A ) or glycine receptors [9,22]. Recent electrophysiological studies using rat brain preparations, however, have shown that taurine application induced long-lasting synaptic potentiation [3,6].…”

Modes of Action of Taurine and Granulocyte Colony-stimulating Factor in Neuroprotection

“…Taurine counteracts excitotoxic upsurges by interacting with GABAA and glycine receptors, thereby increasing the duration of chloride conductance Several lines of evidence indicate that taurine inhibits neurotransmission by binding to ionotropic GABAA and glycine receptors; this has been effectively used for the treatment of Alzheimer's disease. 22,81 Taurine conducts the flow of chloride not by increasing the frequency of the opening of the chloride channels, but by increasing the duration that the channel is open. 82 Very few studies have been conducted on the direct activation of taurine receptors.…”

“…21 Taurine is known for its ability to neuromodularly inhibit postsynaptic taurine receptors and act as an indirect agonist of GABAA and glycine receptors, thereby increasing the duration of chloride channel conductance. 22 Apart from this, the presence of a sodium-dependent taurine transporter (TauT) has been confirmed, and TauT knockouts demonstrate retinal degeneration, reduced olfactory sensitivity, and the manifestation of clinically important age-dependent diseases. 23e25 It is widely accepted that a biochemical mechanism is required to clear a neurotransmitter from the synaptic cleft after neurotransmission in order to maintain levels below toxicity.…”

Intracerebroventricular administration of taurine impairs learning and memory in rats

“…3 Taurine is also widely distributed in the mammalian brain, 4 and it modulates synaptic transmission as an inhibitory neurotransmitter, interacting with gamma-aminobutyric acid type A (GABA A ) or glycine receptors. [5][6][7] Recently, however, Galarreta et al 8 have reported a new aspect of taurine; application of taurine induces a long-lasting enhancement of excitatory postsynaptic potential (EPSP) at the hippocampal CA1 area. Further investigation showed that this long-lasting increase of EPSP had similar features to long-term potentiation, [9][10][11] which is thought to be a basic model for learning and memory.…”