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

本研究旨在探讨GABA合成酶(GAD)与囊泡抑制性氨基酸转运体(VIAAT)功能偶联的调控机制及其在持续性疼痛条件下的调控作用。为此，我们使用配对的全细胞记录分析了脊髓抑制性传递。在持续疼痛的情况下，脊髓神经元的谷氨酸能输入被认为是增加的。应用谷氨酸可显著增加抑制性传递的GABA能成分。另一方面，谷氨酸降低了IPSC的甘氨酸能组分。结果提示，GABA能成分的增加是由于GAD和VIAAT之间的功能耦合所致。神经元活动的抑制减少了这种耦合。目前的结果表明，GABA/甘氨酸能抑制传递是动态的，并且可能能够很容易地改变成分以响应网络活动的变化。

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.