Taurine acts as a glycine receptor agonist in slices of rat inferior colliculus

Han, Xu; Wang, Wei; Tang, Zheng-Quan; Xu, Tian‐Le; Chen, Lin

doi:10.1016/j.heares.2006.07.005

Cited by 22 publications

(14 citation statements)

References 79 publications

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“…Pharmacological applications of taurine can modulate neuronal network activity in vitro and in vivo via the activation of GlyRs, as shown for example in dissociated culture of nucleus accumbens neurons [294], in the ventral tegmental area [286], in the inferior colliculus of young rat [295], and in the rat nucleus accumbens [296]. In addition, low concentrations of taurine can activate extrasynaptic GABA A Rs in the ventrobasal thalamus of adult mice [297].…”

Section: Physiological Roles Of Paracrine/autocrine Release Of Taurinementioning

confidence: 99%

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

et al. 2011

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It is a common and widely accepted assumption that glycine and GABA are the main inhibitory transmitters in the central nervous system (CNS). But, in the past 20 years, several studies have clearly demonstrated that these amino acids can also be excitatory in the immature central nervous system. In addition, it is now established that both GABA receptors (GABARs) and glycine receptors (GlyRs) can be located extrasynaptically and can be activated by paracrine release of endogenous agonists, such as GABA, glycine, and taurine. Recently, non-synaptic release of GABA, glycine, and taurine gained further attention with increasing evidence suggesting a developmental role of these neurotransmitters in neuronal network formation before and during synaptogenesis. This review summarizes recent knowledge about the non-synaptic activation of GABA(A)Rs and GlyRs, both in developing and adult CNS. We first present studies that reveal the functional specialization of both non-synaptic GABA(A)Rs and GlyRs and we discuss the neuronal versus non-neuronal origin of the paracrine release of GABA(A)R and GlyR agonists. We then discuss the proposed non-synaptic release mechanisms and/or pathways for GABA, glycine, and taurine. Finally, we summarize recent data about the various roles of non-synaptic GABAergic and glycinergic systems during the development of neuronal networks and in the adult.

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Section: Physiological Roles Of Paracrine/autocrine Release Of Taurinementioning

confidence: 99%

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

et al. 2011

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“…It has been reported that taurine has various functions including bile acid production [9–12], antiarrhythmic effects [13–15], and oxidant scavenging effects [16]. In central nervous system, taurine has also been reported to modulate calcium homeostasis [17, 18], neuronal excitabilities [19, 20], and excitotoxic cell death [21, 22]. …”

Section: Introductionmentioning

confidence: 99%

Activation of Glycine and Extrasynaptic GABA_AReceptors by Taurine on the Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis

et al. 2013

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The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) has been known for the processing and transmission of orofacial nociceptive information. Taurine, one of the most plentiful free amino-acids in humans, has proved to be involved in pain modulation. In this study, using whole-cell patch clamp technique, we investigated the direct membrane effects of taurine and the action mechanism behind taurine-mediated responses on the SG neurons of the Vc. Taurine showed non-desensitizing and repeatable membrane depolarizations and inward currents which remained in the presence of amino-acid receptors blocking cocktail (AARBC) with tetrodotoxin, indicating that taurine acts directly on the postsynaptic SG neurons. Further, application of taurine at different doses (10 μM to 3 mM) showed a concentration dependent depolarizations and inward currents with the EC50 of 84.3 μM and 723 μM, respectively. Taurine-mediated responses were partially blocked by picrotoxin (50 μM) and almost completely blocked by strychnine (2 μM), suggesting that taurine-mediated responses are via glycine receptor (GlyR) activation. In addition, taurine (1 mM) activated extrasynaptic GABAA receptor (GABAAR)-mediated currents. Taken together, our results indicate that taurine can be a target molecule for orofacial pain modulation through the activation of GlyRs and/or extrasynaptic GABAARs on the SG neurons.

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“…Consistent with the present results, taurine is known to be an agonist at the GlyRs present in cultured rat medullary neurons [30] and it could activate GlyRs composed of ␣ 1 -and ␣ 2 -subunits in the heterologous expression system in vitro [31,32] . In addition, it has been found that taurine acts as a glycine receptor agonist in slices of rat inferior collicus [33] . Taken together, the present results suggest that taurine may activate strychnine-sensitive glycine receptor in mouse brain.…”

Section: Discussionmentioning

confidence: 99%

Taurine Induces Anti-Anxiety by Activating Strychnine-Sensitive Glycine Receptor in vivo

Zhang

Kim²

2007

Ann Nutr Metab

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Taurine has a variety of actions in the body such as cardiotonic, host-defensive, radioprotective and glucose-regulatory effects. However, its action in the central nervous system remains to be characterized. In the present study, we tested to see whether taurine exerts anti-anxiety effects and to explore its mechanism of anti-anxiety activity in vivo. The staircase test and elevated plus maze test were performed to test the anti-anxiety action of taurine. Convulsions induced by strychnine, picrotoxin, yohimbine and isoniazid were tested to explore the mechanism of anti-anxiety activity of taurine. The Rotarod test was performed to test muscle relaxant activity and the passive avoidance test was carried out to test memory activity in response to taurine. Taurine (200 mg/kg, p.o.) significantly reduced rearing numbers in the staircase test while it increased the time spent in the open arms as well as the number of entries to the open arms in the elevated plus maze test, suggesting that it has a significant anti-anxiety activity. Taurine’s action could be due to its binding to and activating of strychnine-sensitive glycine receptor in vivo as it inhibited convulsion caused by strychnine; however, it has little effect on picrotoxin-induced convulsion, suggesting its anti-anxiety activity may not be linked to GABA receptor. It did not alter memory function and muscle activity. Taken together, these results suggest that taurine could be beneficial for the control of anxiety in the clinical situations.

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Taurine acts as a glycine receptor agonist in slices of rat inferior colliculus

Cited by 22 publications

References 79 publications

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

Activation of Glycine and Extrasynaptic GABA_AReceptors by Taurine on the Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis

Taurine Induces Anti-Anxiety by Activating Strychnine-Sensitive Glycine Receptor in vivo

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Taurine acts as a glycine receptor agonist in slices of rat inferior colliculus

Cited by 22 publications

References 79 publications

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

GABAA Receptor and Glycine Receptor Activation by Paracrine/Autocrine Release of Endogenous Agonists: More Than a Simple Communication Pathway

Activation of Glycine and Extrasynaptic GABAAReceptors by Taurine on the Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis

Taurine Induces Anti-Anxiety by Activating Strychnine-Sensitive Glycine Receptor in vivo

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Activation of Glycine and Extrasynaptic GABA_AReceptors by Taurine on the Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis