The Increase of Anterior Pituitary Dopamine in Aging C57BL/6J Female Mice Is Caused by Ovarian Steroids, Not Intrinsic Pituitary Aging
作者:
Nancy Telford,
Charles V. Mobbs,
Yagya N. Sinha,
Caleb E. Finch,
期刊:
Neuroendocrinology
(Karger Available online 1986)
卷期:
Volume 43,
issue 2
页码: 135-142
ISSN:0028-3835
年代: 1986
DOI:10.1159/000124520
出版商: S. Karger AG
关键词: Anterior pituitary;Age;Estradiol;Dopamine;Prolactin secretion
数据来源: Karger
摘要:
We describe how the increase of anterior pituitary dopamine (DA) during aging in female mice is related to altered secretion of ovarian steroids during reproductive senescence. A number of age-correlated neuroendocrine changes in female rodents result from cumulative exposure to ovarian steroids over a lifetime of estrous cycles, or from the altered pattern of ovarian steroid secretion concomitant with reproductive senescence. Pituitary DA has been shown to increase with age in female rats. To examine how the age-correlated increase of pituitary DA may depend on estradiol (E2), we measured pituitary DA and serum prolactin (PRL) in the following groups of female mice: young (7 months) cycling, middle-aged (14 months) cycling and non-cycling, old (17 months) non-cycling, old (17 months) ovariectomized (OVX) at 4 months, and young mice given 0.2 mg E2 valerate or E2 implants. Mice from some of these groups were OVX 1, 4 or 8 weeks before sacrifice. Compared with young controls, 14-month-old cycling or non-cycling mice had 3-fold higher pituitary DA, and 17-month-old non-cycling mice had 5-fold higher pituitary DA. OVX for 2 or 13 months before sacrifice abolished the effect of age; OVX of young mice had no effect on pituitary DA. Three weeks after implantation of E2 into OVX young mice or 7 weeks after injection of E2 valerate in intact young mice, pituitary DA was elevated. The E2-sensitive fraction of pituitary DA does not appear to decrease PRL secretion. We conclude that the age-correlated increase in pituitary DA is primarily dependent upon the effectively enhanced estrogenic stimulation concomitant with reproductive senescence, rather than upon intrinsic pituitary aging or irreversible effects from exposure to E2 over a lifetime of estrous cycles.
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