| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Research Abstract |
In this study, we investigated the role of acid sensing ion channel (ASIC) and the transient receptor potential vanilloid subfamily member 1 (TRPV1) for pathophysiology of migraine. In addition to vascular dysfunction, the neurogenic inflammation of the dura mater innervated by the trigeminal ganglion is considered to be related to migraine pathophysiology. We demonstrated the existence of the TRPV1 receptor in the dura mater and the trigeminal ganglion in this project. Furthermore, our data showed that the nociceptive stimulation of TRPV1 receptors in the dura mater caused the phosphorylation of ERK, which is in response to the noxious stimulation of peripheral TRPV1 receptors in the trigeminal ganglion in vivo. We also observed the phosphorylation of ERK in vitro. As such phosphorylation was found to occur rapidly after TRPV1 stimulation, we surmised that ERK phosphorylation can serve as sensitive marker of nociception at the level of the trigeminal ganglion. We also observed the developmental pattern of the diploic veins and the relationship between the diploic veins and the dural TRPV1 receptor. Many dural TRPV1 receptor immunoreactive nerve fibers were observed over the diploic veins and these finding indicated the possibility that heat from the diploic veins may affect to the threshold of the TRPV1 receptor
|
