Project/Area Number |
22500390
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Laboratory animal science
|
Research Institution | Showa University |
Principal Investigator |
ARATA Satoru 昭和大学, 遺伝子組換え実験室, 准教授 (20159502)
|
Co-Investigator(Kenkyū-buntansha) |
ONIMARU Hiroshi 昭和大学, 医学部, 准教授 (30177258)
NAKAMACHI Tomoya 昭和大学, 遺伝子組換え実験室, 助教 (30433840)
畠 あずさ 昭和大学, 動物実験施設, 技術員 (20568290)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | 乳幼児突然死症候群(SIDS) / 呼吸中枢障害マウスモデル / Pituitary adenylate cyclase activating polypeptide(PACAP) / SIDS / PACAP / 呼吸中枢 / 低酸素受容体 / 中枢性呼吸疾患 / 疾患モデルマウス |
Research Abstract |
Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuropeptide expressed widely in nervous tissues. PACAP knockout (-/-) mice display a sudden infant death syndrome (SIDS)-like phenotype, although the underlying physiological mechanism to explain this remains unclear. Here, we reporton the presence of abnormal respiratory activity in PACAP -/- mice under hypoxic conditions, which provides a basis for the SIDS-like phenotype. PACAP -/- mice display a lowered baseline respiratory activity compared with wild-type animals, and an abnormal response to hypoxia. Histological and real time PCR analyses indicated that the catecholaminergic system in the medulla was impaired in PACAP-/- mice, suggesting that endogenous PACAP affects respiratory centers in the medulla via its action on the catecholaminergic system. We propose that disruption of this system may beinvolved in the sudden infant death-like phenotype of PACAP -/- mice. Thus, disorders of the catecholaminergic system involved with O_2sensing could be implicated in underlying neuronal mechanisms responsible for SIDS.
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