1999 Fiscal Year Final Research Report Summary
Cellular and extracellular regulatory mechanisms for hypothalamic CRH gene expression
| Project/Area Number |
10671029
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Endocrinology
|
|---|
| Research Institution | TOHOKU UNIVERSITY |
|---|
Principal Investigator |
ITOI Keiichi Tohoku University Hospital, Research Associate, 医学部・附属病院, 助手 (60232427)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SUGAWARA Akira Tohoku University Hospital, Research Associate, 医学部・附属病院, 助手 (90270834)
|
|---|
| Project Period (FY) |
1998 – 1999
|
| Keywords | Hypothalamus / CRH / gene / in situ hybridization / rat / A kinase / C kinase / transcription |
|---|
| Research Abstract |
The hypothalamic-pituitary-adrenal axis is necessary to maintain the internal milieu of living organisms. Norepinephrine (NE) has been shown to stimulate CRH gene expression in the paraventricular nucleus of the hypothalamus (PVN). On the other hand, CRH colocalizes with arginine vasopressin (AVP) in the parvocellular division of the PVN. We investigated the effect of NE on primary transcripts of CRH and AVP in the PVN by microinjection of NE directly into the PVN of conscious rats. NE stimulated CRH gene transcription, whereas it had no significant effect on AVP gene transcription. We reported the same experiments using rats, adrenalectomized and supplemented with low-dose corticosterone. It became clear that glucocorticoid affects CRH- and AVP gene in a different manner, AVP gene being more sensitive to the circulating glucocorticoid in this acute experimental paradigm. Furthermore, TPA stimulated CRH gene expression in a human neuroblastoma cell line, BE(2)-M17, suggesting the physiological role of the PKC pathway in the regulation of CRH gene expression.
|
Research Products
(12 results)
