| Project/Area Number |
18500251
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Neuroscience in general
|
|---|
| Research Institution | National Institute for Basic Biology |
|---|
Principal Investigator |
WATANABE Eiji National Institute for Basic Biology, Center for Transgenic Animals and plants, Associate Professor (30250252)
|
|---|
| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥4,020,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
|---|
| Keywords | glia / sodium / sensor / homeostasis / channel / circumventricular organs / gene-targetine mouse / cell culture |
|---|
| Research Abstract |
Sodium homeostasis is crucial for life and Na-levels in body fluids are constantly monitored in the brain. The subfornical organ (SFO) is the center of the sensing responsible for the control of Na-intake behavior, where Nax channels are expressed in specific glial cells as the sodium-level sensor. Here, we show direct interaction between Nax channels and subunits of Na+/K+-ATPase, which brings about Na-dependent activation of the metabolic state of the glial cells. The metabolic enhancement leading to extensive lactate production was observed in the SFO of wild-type mice, but not of the Nax-knockout mice. Furthermore, lactate, as well as Na, stimulated the activity of GABAergic neurons in the SFO. These results suggest that the information on a physiological increase of the Na level in body fluids sensed by Nax in glial cells is transmitted to neurons by lactate as a mediator to regulate neural activities of the SFO.
|
