2013 Fiscal Year Final Research Report
Contribution of the spontaneous calcium rhythm to the state of the striatal network
| Project/Area Number |
23590255
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General physiology
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
OSANAI Makoto 東北大学, 医学(系)研究科(研究院), 准教授 (90286419)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Keywords | カルシウム振動 / 大脳基底核 / カルシウムイメージング / 代謝型グルタミン酸受容体 / IP3 受容体 / ニューロン・グリア相互作用 / パーキンソン病 / 細胞間相関 |
|---|
| Research Abstract |
Ca2+ is a universal signal transduction molecule. To characterize Ca2+ signaling in striatal cells, spontaneous Ca2+ rhythms were examined in slice preparations. In both neurons and astrocytes of the striatum, spontaneous slow and long-lasting intracellular Ca2+ rhythms, which lasted up to 200 s, were found. Depletion of the intracellular Ca2+ store and the blockade of IP3 receptors reduced the transient rate of the Ca2+ rhythm, and an mGluR5 antagonist blocked the Ca2+ rhythms in both neurons and astrocytes. Thus, the mGluR5-IP3 signal cascade is the primary contributor to the Ca2+ rhythm in both neurons and astrocytes. The Ca2+ rhythm features multicellular synchrony, and both neurons and astrocytes participate in the synchronous activity. Therefore, the Ca2+ rhythm may involve in the neuron-glia interaction in the striatum. In the simulation study, we found that the Ca2+ rhythm can modulate the firing properties of the medium spiny projection neurons via Ca2+-activated K+ channels.
|
