Functional coupling between GABA synthetic enzyme and vesicular GABA transporter and its modulation by persistent pain

本研究的目的是确定GABA合成酶（GAD）和囊泡抑制性氨基酸转运蛋白（VIAAT）之间的功能耦合的调节机制，以及其在持续性疼痛条件下的调制。为此，我们分析了脊髓抑制性传输使用配对的全细胞记录。在持续性疼痛条件下，对脊髓神经元的谷氨酸能输入被认为增加。谷氨酸的应用显著增加了抑制性传递的GABA能成分。另一方面，谷氨酸减少了IPSC的甘氨酸能成分。结果表明，GABA能成分的增加是由于GAD和VIAAT之间的功能偶联。抑制神经元的活动减少耦合。目前的结果表明，GABA/甘氨酸能抑制传输是动态的，并可能能够很容易地改变组件在网络活动的变化作出反应。

The aim of this study was to determine the regulatory mechanisms underlying functional coupling between GABA synthetic enzyme(GAD) and vesicular inhibitory amino acid transporter(VIAAT), and its modulation under persistent pain conditions. For this purpose, we analyzed the spinal inhibitory transmission using paired whole-cell recordings. Glutamatergic inputs onto spinal neurons are thought to be increased under persistent pain conditions. Application of glutamate markedly increased the GABAergic component of inhibitory transmission. On the other hand, glutamate reduced glycinergic component of IPSC. The results suggest the increase in GABAergic component is due to the functional coupling between GAD and VIAAT. The inhibition of neuronal activity reduced the coupling. The present results suggest that the GABA/glycinergic inhibitory transmission is dynamic, and may be able to easily change the component in response to changes in network activity.