Project/Area Number |
09671689
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Kochi Medical School |
Principal Investigator |
OKATANI Yuji Kochi Medical School, Associate professor, 医学部, 助教授 (70145142)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
|
Keywords | melatonin / pineal gland / estrogen / puberty |
Research Abstract |
We have demonstrated that estrogen modulates the nocturnal synthesis of melatonin by the pineal gland in the peripubertal female rat and suggested that the decline in melatonin synthesis during the puberty may be related to the increase in the level of endogenous estrogen being secreted by the maturing ovary. This study was designed to determine the mechanism for the effect of estrogen on melatonin synthesis in female rats during the peripubertal period. Accordingly, we evaluated the effects of long-term estrogen deficit and of estrogen stimulation on nocturnal levels of melatonin, N-acetylserotonin (NAS) and on N-acetyltransferase (NAT) and liydroxyindole-O-methyltransferaise (HIOMT) activity. A peak in the pineal levels of melatonin and NAS and in NAT activity was observed in control rats at 6 weeks. HIOMT activity increased from week 4 to 6 and remained unchanged after. Ovariectomy at week 4 led to significant increases in the levels of melatonin and of NAS and NAT in activity at week 8. NAT activity week 10 resembled that of control animals, but levels of melatonin and NAS were slightly elevated. Ovariectomy did not affect HIOMT activity. Subcutaneous infection of E_2B significantly decreased the levels of melatonin and NAS and of NAT activity at week 4, as compared with those in control rats. E_2B suppressed the ovariectomy-induced elevation of levels of melatonin and NAS and of NAT activity, similar to the effect in control rats. E_2B did not affect HIOMT activity. Furthermore, changes in the activity of adenylate cyclase resembled those observed with NAT at the same time. Our results suggest that estrogen modulates the nocturnal synthesis of melatonin in the pineal gland in peripubertal female rats. The inhibitory effect of estrogen on melatonin synthesis appeared to be mediated by the modulation of NAT activity. The norepinephrine-induced stimulation of pineal adenylate cyclase activity may be also affected by estrogen.
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