| Project/Area Number |
18300216
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Sports science
|
|---|
| Research Institution | University of Tsukuba |
|---|
Principal Investigator |
SOYA Hideaki University of Tsukuba, Graduate School of Comprehensive Human Sciences, Associate Professor (50221346)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
FUJIKAWA Takashi Mie University, Graduate School of Medicine, Lecturer (60293776)
ONAKA Tatsushi Jichi Medical University, School of Medicine, Professor (90177254)
|
|---|
| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥17,910,000 (Direct Cost: ¥15,300,000、Indirect Cost: ¥2,610,000)
Fiscal Year 2007: ¥11,310,000 (Direct Cost: ¥8,700,000、Indirect Cost: ¥2,610,000)
Fiscal Year 2006: ¥6,600,000 (Direct Cost: ¥6,600,000)
|
|---|
| Keywords | PrRP / Running exercise / ACTH / Lactate / Brain stem / Hypothalamus / AVP / Fos / 走運動ストレス / 脳室内投与 / Lactate |
|---|
| Research Abstract |
Running stimulates ACTH release when speed is beyond the lactate threshold (LT), the breakpoint for blood lactate accumulation appears to be around 50-60% of maximal oxygen uptake, defined as running stress. Although the exact brain mechanism underlying the running-induced ACTH response is unknown, the ventrolateral medulla (VLM) and the nucleus of the solitary tract (NTS) that project to the hypothalamic paraventricular nucleus would have crucial role in regulating running stress. Prolactin releasing peptide (PrRP) was recently isolated and found to be produced by the VLM, NTS and dorsomedial hypothalamic nucleus. Intracerebroventricular administration of PrRP stimulates ACTH release and the Fos protein accumulation in PrRP neurons increased under stress conditions suggest that PrRP neurons play a role in running stress-induced ACTH response. First, we previously found that Fos protein accumulation in A1 noradrenaline neurons that contain PrRP increased depends on running speed, espec
… More
ially just above the LT (Exp.1). In the Exp.2, first we found that Fos accumulation increased depend on running speed (Exp.2). Further, we found that immunoneutralization of brain PrRP with use of icv administration with monoclonal antibody for PrRP significantly enhances ACTH and blood lactate levels increases in response to running stress (Exp.3). On the contrary, i.c.v. treatment with low dose of PrRP (1nmol) caused opposite effects than that of the immunoneutralization (Exp.4). This shows PrRP partially mediates ACTH release response to running stress through inhibitory action on the central nervous system. In the Exp.5, we hypothesized that this neuronal mechanism by which PrRP reduces blood lactate and ACTH responses would be exerted via inhibitory action on the hypothalamic AVP neurons, especially in the AVP neurons in the parvocellular paraventricular nucleus (pPVN) and supraoptic nucleus (SON). As the results, if administered (icv) low dose of PrRP (1nmol) caused dramatic decrease in Fos accumulation in the pPVN-and SON-AVP positive neurons in response to running stress. The present results suggest that brain PrRP suppress the running stress-induced lactate and ACTH responses by acting in the hypothalamus : the inhibitory action was exerted in the pPVN-and SON-AVP neurons. Thus, we thus propose a new hypothesis that PrRP may have a significant role to maintain the expenditure of exercise to be high. Less
|
