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Low dose chronic estradiol-17beta Ex...

Gilbreath, Ebony Turner.

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Low dose chronic estradiol-17beta Exposure induces ovarian pathology and inhibits tuberoinfundibular dopaminergic neuronal function by inducing a proinflammatory state within the arcuate nucleus.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Low dose chronic estradiol-17beta Exposure induces ovarian pathology and inhibits tuberoinfundibular dopaminergic neuronal function by inducing a proinflammatory state within the arcuate nucleus./
作者:	Gilbreath, Ebony Turner.
面頁冊數:	174 p.
附註:	Source: Dissertation Abstracts International, Volume: 72-07, Section: B, page: .
Contained By:	Dissertation Abstracts International72-07B.
標題:	Biology, Neuroscience. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3453109
ISBN:	9781124610566

Low dose chronic estradiol-17beta Exposure induces ovarian pathology and inhibits tuberoinfundibular dopaminergic neuronal function by inducing a proinflammatory state within the arcuate nucleus.
Gilbreath, Ebony Turner.

Low dose chronic estradiol-17beta Exposure induces ovarian pathology and inhibits tuberoinfundibular dopaminergic neuronal function by inducing a proinflammatory state within the arcuate nucleus. - 174 p.

Source: Dissertation Abstracts International, Volume: 72-07, Section: B, page: .

Thesis (Ph.D.)--Michigan State University, 2011.

Estrogen exposure is known to inhibit tuberoinfundibular dopaminergic (TIDA) neuronal function and cause hyperprolactinemia which can lead to the development of mammary and pituitary tumors. Dopamine produced by TIDA neurons acts on lactotrophs in the anterior pituitary gland to provide tonic inhibition of prolactin release. Therefore, if TIDA neuronal function is inhibited by estrogen, there is a decrease in dopamine (DA) release into the median eminence (ME), loss of inhibition to prolactin, and a resulting state of hyperprolactinemia. The mechanism by which estrogen exerts this effect has not been elucidated. We hypothesized that chronic exposure to a low dose of estradiol-17beta (E2) would cause an increase in IL-1beta and nitrate levels in the arcuate nucleus (AN), where TIDA neuronal cell bodies are located, and cause direct damage to TIDA function through nitration of tyrosine hydroxylase (TH), which is the rate-limiting enzyme in DA synthesis. To test this hypothesis, we exposed intact and ovariectomized Sprague-Dawley rats to E2 by subcutaneously implanting them with slow-release E2 pellets (20ng/day) for 90 days. After exposure, animals were sacrificed and serum was analyzed for prolactin, the ME for dopamine and nitrated tyrosine hydroxylase (nTH), and the AN was assessed for IL-1a and nitrate levels. Our results demonstrate that E2 exposure increased serum prolactin, decreased DA levels in the ME, increased IL-1a and nitrate levels in the AN and increased the ratio of nTH to TH in the ME. These findings provide strong evidence that chronic exposure to a low level of E2 induces a proinflammatory state within the AN and this may be a mechanism by which E2 inhibits TIDA activity to cause hyperprolactinemia.

ISBN: 9781124610566Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Low dose chronic estradiol-17beta Exposure induces ovarian pathology and inhibits tuberoinfundibular dopaminergic neuronal function by inducing a proinflammatory state within the arcuate nucleus.
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100 1 $a Gilbreath, Ebony Turner. $3 1684913
245 1 0 $a Low dose chronic estradiol-17beta Exposure induces ovarian pathology and inhibits tuberoinfundibular dopaminergic neuronal function by inducing a proinflammatory state within the arcuate nucleus.
300 $a 174 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-07, Section: B, page: .
500 $a Advisers: Puliyur S. MohanKumar; Sheba MohanKumar.
502 $a Thesis (Ph.D.)--Michigan State University, 2011.
520 $a Estrogen exposure is known to inhibit tuberoinfundibular dopaminergic (TIDA) neuronal function and cause hyperprolactinemia which can lead to the development of mammary and pituitary tumors. Dopamine produced by TIDA neurons acts on lactotrophs in the anterior pituitary gland to provide tonic inhibition of prolactin release. Therefore, if TIDA neuronal function is inhibited by estrogen, there is a decrease in dopamine (DA) release into the median eminence (ME), loss of inhibition to prolactin, and a resulting state of hyperprolactinemia. The mechanism by which estrogen exerts this effect has not been elucidated. We hypothesized that chronic exposure to a low dose of estradiol-17beta (E2) would cause an increase in IL-1beta and nitrate levels in the arcuate nucleus (AN), where TIDA neuronal cell bodies are located, and cause direct damage to TIDA function through nitration of tyrosine hydroxylase (TH), which is the rate-limiting enzyme in DA synthesis. To test this hypothesis, we exposed intact and ovariectomized Sprague-Dawley rats to E2 by subcutaneously implanting them with slow-release E2 pellets (20ng/day) for 90 days. After exposure, animals were sacrificed and serum was analyzed for prolactin, the ME for dopamine and nitrated tyrosine hydroxylase (nTH), and the AN was assessed for IL-1a and nitrate levels. Our results demonstrate that E2 exposure increased serum prolactin, decreased DA levels in the ME, increased IL-1a and nitrate levels in the AN and increased the ratio of nTH to TH in the ME. These findings provide strong evidence that chronic exposure to a low level of E2 induces a proinflammatory state within the AN and this may be a mechanism by which E2 inhibits TIDA activity to cause hyperprolactinemia.
520 $a Additionally, estrogen is known to induce ovarian follicular cysts. Exposure to estrogen has been implicated as a model for polycystic ovary syndrome (PCOS) in women. However, most studies claiming this association, have primarily focused on the ovarian morphologic phenotype and have not thoroughly assessed other clinical parameters observed with PCOS. We explored whether our paradigm of E2 exposure could cause changes in ovarian morphology and hormonal profiles similar to that of PCOS. Adult female rats were implanted with slow-release E2 pellets for 30, 60 (, or 90 days. At the end of treatment, testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured, ovaries were analyzed histomorphologically and immunohistochemistry for CD68 (a macrophage marker) and Mullerian inhibiting substance (MIS) was assessed.. We found that follicular size increased with E2 exposure and number of corpora lutea (CL) decreased in an exposure-dependent manner indicating failure of ovulation. There was an E2 associated increase in follicular degeneration and CD68 positive cells, and a decrease in MIS. Testosterone levels decreased in a duration dependent manner and the ratio of LH to FSH remained unaffected. While ovarian changes observed in this model are similar to that seen in PCOS, the hormonal profiles arenot, and we therefore determined that this may not be a true model for this condition.
590 $a School code: 0128.
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Biology, Endocrinology. $3 1682242
650 4 $a Health Sciences, Pathology. $3 1017854
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710 2 $a Michigan State University. $b Pathology. $3 1684900
773 0 $t Dissertation Abstracts International $g 72-07B.
790 1 0 $a MohanKumar, Puliyur S., $e advisor
790 1 0 $a MohanKumar, Sheba, $e advisor
790 1 0 $a Agnew, Dalen $e committee member
790 1 0 $a Fink, Gregory $e committee member
790 1 0 $a Nunez, Antonio $e committee member
790 $a 0128
791 $a Ph.D.
792 $a 2011
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3453109