| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Research Abstract |
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.
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