Role of calmoduline binding protein in the mechanism of prolactin secretion
| Project/Area Number |
62570754
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Osaka University. Department of Obstetrics & Gynecololy |
|---|
Principal Investigator |
KENJI Hirota Osaka University Medical School. Research fellow, 医学部, 助手 (00189888)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KADOWAKI Kozo Osaka University Medical School. Research fellow, 医学部, 助手 (60194875)
MIYAKE Akira Osaka University Medical School. Assistant Professor, 医学部, 講師 (90093468)
|
|---|
| Project Period (FY) |
1987 – 1988
|
| Project Status |
Completed (Fiscal Year 1988)
|
| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
|---|
| Keywords | Prolactin / TRH / GTP binding protein / Calmodulin / IAP / 下垂体細胞 / アラキドン酸 / カルスペクチン / phospholipase A_2 / 下垂体前葉 / 視床下部 / カルシウム |
|---|
| Research Abstract |
It is well known that prolactin is released from pituitary gland by TRH and inhibited by dopamine. We tried to clarify the role of calcium and calmodulin in prolactin release by TRH, and the role of guanosine trisphosphate (GTP) binding protein in inhibitory mechanism of PRL by dopamine. Pituitary cells and hypothalamic cells were used for the experiment. Maitotoxin induced Ca2+ influx, arachidonate and prolactin release. These results showed Ca2+ influx induce prolaction release. Prolactin secretion was suppressed by W7, which is an antagonist of calmodulin. Phospholipase A2, activated by Ca2+, inducedarachidonate and prolactin. As a conclusion, we showed that Ca2+ influx stimulates prolactin secretion through calmodulin and phospholipase A2. On the other hand, prolactin secretion is inhibited by dopamine. we tried to clarified whether the islet-activating protein (IAP) sensitive guano sine trisphosphate (GTP) protein is involved in TRH or dopamine receptor. Although IAP did not stimulate prolactin release nor inhibited prolactin release stimulated TRH or phospholipase A2 or arachidonate. IAP in activated dopamine action, which suppressed prolactin secretion stimulated by TRH. These results show that dopamine suppressed prolactin secretion through IAP sensitive GTP protein.
|
Report
(3 results)
Research Products
(24 results)
