Evaluation of the role played by neurosteroids in the ADH-releasing mechanism mediated by forebrain receptors for amino-acid transmitters
Project/Area Number |
21590252
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
|
Research Institution | Niigata University |
Principal Investigator |
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 第三脳室前腹側部(AV3V) / GABA(γ-アミノ酪酸) / グルタミン酸(Glu) / 神経ステロイト / 抗利尿ホルモン(ADH) / 浸透圧上昇 / 低容量減少 / 心血管系 / AV3V / 神経ステロイド / ADH / 血液量減少 / 血糖値 |
Research Abstract |
An increase in plasma osmolality and a decrease in blood volume are primary factors to facilitate ADH secretion. Both stimulus excites hypothalamic ADH-releasing cells by causing inactivation of the GABA(A) receptor in a forebrain region called the anteroventral third ventricle(AV3V). It is well known that the GABA(A) receptor includes a lot of subtypes, among which there exists a subtype whose binding affinity to GABA is highly affected by steroids generated in the brain tissue(neurosteroids, NS). However, topical infusions in the AV3V with NS or an inhibitor for the synthesis of NS affected neither basal ADH release nor stimulated ADH secretion by pharmacological blockade of the GABA(A) receptor, plasma hyperosmolality or blood hypovolemia. These results suggest that AV3V GABA(A) receptors involved in ADH secretion may not be regulated acutely at least by NS.
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Report
(4 results)
Research Products
(65 results)