Effect of Taurine on the Concentrations of Glutamate, GABA, Glutamine and Alanine in the Rat Striatum and Hippocampus (original) (raw)
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Long-lasting enhancement of corticostriatal neurotransmission by taurine
European Journal of Neuroscience, 2002
Taurine occurs at high concentrations in the forebrain and its distribution varies with (patho)physiological conditions; however, its role in neural function is poorly understood. We have now characterized its effects on corticostriatal synaptic transmission. Bath application of taurine (10 mM) to slices obtained from mice and rats exerted a biphasic action on corticostriatal ®eld potentials. The fast and reversible inhibition by taurine was accompanied by a depolarization and conductance increase in medium spiny neurons and was sensitive to g-aminobutyric acid (GABA) A and glycine receptor (GlyR) antagonists. A long-lasting enhancement (LLE TAU ) of ®eld potentials was recorded after taurine withdrawal. The LLE TAU was not prevented by N-methyl-D-aspartate (NMDA)-or by GABA A receptor-antagonists, but was sensitive to the GlyR-antagonist strychnine and blocked by the competitive taurine uptake inhibitor guanidinoethylsulphonate (GES, 1 mM). GES at 10 mM evoked an enhancement of ®eld potentials similar to LLE TAU . LLE TAU depended on protein kinase C activation as it was blocked by chelerythrine, but was unaffected by tri¯uoperazine, and thus independent of calmodulin. LLE TAU was signi®cantly smaller in juvenile than in mature rodents. Activation of GlyRs and the speci®c taurine transporter by taurine evoke a long-lasting enhancement of corticostriatal transmission.
Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update
Neurochemical Research, 2005
Taurine appears to have multiple functions in the brain participating both in volume regulation and neurotransmission. In the latter context it may exert its actions by serving as an agonist at receptors of the GABAergic and glycinergic neurotransmitter systems. Its interaction with GABA A and GABA B receptors as well as with glycine receptors is reviewed and the physiological relevance of such interactions is evaluated. The question as to whether local extracellular concentrations of taurine are likely to reach the threshold level for the pertinent receptor populations cannot presently be answered satisfactorily. Hence more sophisticated analytical methods are warranted in order to obtain a definite answer to this important question.
Taurine as a Modulator of Excitatory and Inhibitory Neurotransmission
Neurochemical Research, 2004
We present data that summarize our findings on the role of taurine in the central nervous system and in particular taurine's interaction with the inhibitory and excitatory systems. In taurine-fed mice, the expression level of glutamic acid decarboxylase (GAD), the enzyme responsible for GABA synthesis, is elevated. Increased expression of GAD was accompanied by increased levels of GABA. We also found in vitro, that taurine regulates neuronal calcium homeostasis and calciumdependent processes, such as protein kinase C (PKC) activity. This calcium-dependent kinase was regulated by taurine, whereas the activity of protein kinase A (PKA), a cAMP-dependent, calciumindependent kinase, was not affected. Furthermore, as a consequence of calcium regulation, taurine counteracted glutamate-induced mitochondrial damage and cell death.
Taurine as osmoregulator and neuromodulator in the brain
Metab Brain Dis, 1996
Taurine has been assumed to function as an osmoregulator and neuromodulator in the brain . The pertinent studies are now reviewed in an attempt to formulate a unifying hypothesis as to how taurine could simultaneously act in both roles . Neuromodulatory actions of taurine may also underlie its protective effects against neuronal overexcitation and glutamate agonist-induced neurotoxicity .
Role of taurine in the central nervous system
Journal of Biomedical Science, 2010
Taurine demonstrates multiple cellular functions including a central role as a neurotransmitter, as a trophic factor in CNS development, in maintaining the structural integrity of the membrane, in regulating calcium transport and homeostasis, as an osmolyte, as a neuromodulator and as a neuroprotectant. The neurotransmitter properties of taurine are illustrated by its ability to elicit neuronal hyperpolarization, the presence of specific taurine synthesizing enzyme and receptors in the CNS and the presence of a taurine transporter system. Taurine exerts its neuroprotective functions against the glutamate induced excitotoxicity by reducing the glutamate-induced increase of intracellular calcium level, by shifting the ratio of Bcl-2 and Bad ratio in favor of cell survival and by reducing the ER stress. The presence of metabotropic taurine receptors which are negatively coupled to phospholipase C (PLC) signaling pathway through inhibitory G proteins is proposed, and the evidence supporting this notion is also presented.
Modulation of taurine release by glutamate receptors and nitric oxide
Progress in Neurobiology, 2000
Taurine is held to function as a modulator and osmoregulator in the central nervous system, being of particular importance in the immature brain. In view of the possible involvement of excitatory pathways in the regulation of taurine function in the brain, the interference of glutamate receptors with taurine release from dierent tissue preparations in vitro and from the brain in vivo is of special interest. The release of taurine from the brain is enhanced by glutamate receptor agonists. This enhancement is inhibited by the respective receptor antagonists both in vitro and in vivo. The ionotropic N-methyl-D-aspartate (NMDA) and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor agonists appear to be the most eective in enhancing taurine release, their eects being receptor-mediated. Kainate is less eective, particularly in adults. Of the glutamate receptors, the NMDA class seems to be the most susceptible to modulation by nitric oxide. Nitric oxide also modulates taurine release, enhancing the basal release in both immature and mature hippocampus, whereas the K + -stimulated release is generally inhibited. Metabotropic glutamate receptors also participate in the regulation of taurine release, group I metabotropic glutamate receptors potentiating the release in the developing hippocampus, while group III receptors may be involved in the adult. Under various cell-damaging conditions, including ischemia, hypoxia and hypoglycemia, taurine release is enhanced, together with an enhanced release of excitatory amino acids. The increase in extracellular taurine upon excessive stimulation of glutamate receptors and under cell-damaging conditions may serve as an important protective mechanism against excitotoxicity, being particularly eective in the immature brain. 7
Brain Research, 1991
While excitatory amino acids (EAAs) are known to evoke the release of taurine in the hippocampus, we have found that taurine is localized primarily in dendrites and only to a lesser extent in terminals in this region. To determine whether taurine is released as a neurotransmitter by non-toxic concentrations of EAAs, or exclusively as a neuroprotectant in response to excitotoxicity, we monitored the release of amino acids from hippocampal slices during simultaneous electrophysiological recording in the CA1 region to assess tissue viability. Nmethyl-D-aspartate (NMDA) was the most potent of the EAA agonists tested for stimulating release of taurine. Exposure of slices to 120/~M NMDA increased the concentration of taurine in the perfusate to 1325% of its basal value. Kainate (KA) at a concentration of 128/~M increased taurine to 543% of baseline while quisqualate (Quis) at a concentration of 120#M increased taurine to only 202% of its baseline value. Release of taurine in response to NMDA and KA peaked during the period when the concentration of the agonist was declining in the bath and did not return to its baseline value until 20 min after removal of the agonist. Increases in release of taurine were associated with concentrations of NMDA, KA, and Quis that caused an incomplete recovery of the CA1 field potential. These results suggest that taurine is primarily released by concentrations of glutamate receptor agonists that exhibit evidence of excitotoxicity in the CA1 region.
Journal of Neurochemistry, 1984
Abstract: The effect of guanidinoethane sulfonic acid (GES), an inhibitor of taurine uptake, was examined with respect to endogenous amino acids in the hippocampus of the freely moving rabbit. GES increased the extracellular levels of both taurine and phosphoethanolamine (PEA), other amino acids being unaffected. However, long-term oral administration of GES selectively reduced endogenous taurine levels. The effect of GES on PEA appeared to be a consequence of the elevated extracellular taurine as exogenously administered taurine per se increased PEA levels in the extracellular space. The findings are discussed in conjunction with the proposed membrane-stabilizing effects of taurine.
Mechanisms of long-lasting enhancement of corticostriatal neurotransmission by taurine
Advances in experimental medicine and biology, 2006
The long-lasting enhancement of corticostriatal neurotransmission by taurine, LLE-TAU represents a complex phenomenon requiring concurrent activation of glycine, DA and Ach receptors as well as taurine uptake. The data on the mechanisms of corticostriatal LLE-TAU can be integrated in the following scheme. Taurine interaction with glycine and GABAA receptors causes depolarization of striatal medium spiny cells (Chepkova et al., 2002) which is enhanced by taurine electrogenic uptake by TauT (Sarkar et al., 2003). This depolarization leads to Ca2+ entry via low voltage gated Ca2+ channels. Muscarinic M1 receptors are expressed in medium spiny neurons (Yan et al., 2001) and regulate their excitability mostly via phospholipase C (PLC)/PKC cascade (Lin et al., 2004). Concurrent activation of M1 and PLC-coupled D1 receptors (O'Sullivan et al., 2004) can amplify Ca2+ signal via IP3- stimulated Ca2+ release from intracellular stores and stimulate PKC.