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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus.
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Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus.

机译：牛磺酸是丘脑中突触外GABA（A）受体的有效激活剂。

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摘要

Taurine is one of the most abundant free amino acids in the brain. In a number of studies, taurine has been reported to activate glycine receptors (Gly-Rs) at moderate concentrations ( or = 100 microM), and to be a weak agonist at GABA(A) receptors (GABA(A)-Rs), which are usually activated at high concentrations ( or = 1 mM). In this study, we show that taurine reduced the excitability of thalamocortical relay neurons and activated both extrasynaptic GABA(A)-Rs and Gly-Rs in neurons in the mouse ventrobasal (VB) thalamus. Low concentrations of taurine (10-100 microM) decreased neuronal input resistance and firing frequency, and elicited a steady outward current under voltage clamp, but had no effects on fast inhibitory synaptic currents. Currents elicited by 50 microM taurine were abolished by gabazine, insensitive to midazolam, and partially blocked by 20 microM Zn2+, consistent with the pharmacological properties of extrasynaptic GABA(A)-Rs (alpha4beta2delta subtype) involved in tonic inhibition in the thalamus. Tonic inhibition was enhanced by an inhibitor of taurine transport, suggesting that taurine can act as an endogenous activator of these receptors. Taurine-evoked currents were absent in relay neurons from GABA(A)-R alpha4 subunit knock-out mice. The amplitude of the taurine current was larger in neurons from adult mice than juvenile mice. Taurine was a more potent agonist at recombinant alpha4beta2delta GABA(A)-Rs than at alpha1beta2gamma2 GABA(A)-Rs. We conclude that physiological concentrations of taurine can inhibit VB neurons via activation of extrasynaptic GABA(A)-Rs and that taurine may function as an endogenous regulator of excitability and network activity in the thalamus.
机译：牛磺酸是大脑中最丰富的游离氨基酸之一。在许多研究中，据报道牛磺酸可在中等浓度（>或= 100 microM）激活甘氨酸受体（Gly-Rs），并且在GABA（A）受体（GABA（A）-Rs）上是弱激动剂。 ，通常在高浓度（>或= 1 mM）下被激活。在这项研究中，我们显示牛磺酸降低了丘脑皮质中枢神经元的兴奋性，并激活了小鼠腹基底（VB）丘脑中神经元的突触外GABA（A）-Rs和Gly-Rs。低浓度的牛磺酸（10-100 microM）会降低神经元输入电阻和放电频率，并在电压钳制下引起稳定的向外电流，但对快速抑制的突触电流没有影响。由50 microM牛磺酸引起的电流被gabazine废除了，对咪达唑仑不敏感，并被20 microM Zn2 +部分阻断，这与丘脑中抑制补品的突触外GABA（A）-Rs（alpha4beta2delta亚型）的药理学性质一致。牛磺酸转运的抑制剂可增强对牛磺酸的抑制作用，表明牛磺酸可作为这些受体的内源性激活剂。从GABA（A）-R alpha4亚基敲除小鼠的接力神经元中不存在牛磺酸引起的电流。在成年小鼠的神经元中，牛磺酸电流的幅度大于未成年小鼠。牛磺酸在重组alpha4beta2delta GABA（A）-Rs上比在alpha1beta2gamma2 GABA（A）-Rs上更有效。我们得出的结论是，牛磺酸的生理浓度可以通过突触外GABA（A）-Rs的激活来抑制VB神经元，并且牛磺酸可能充当丘脑中兴奋性和网络活动的内源性调节剂。

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