Ovarian steroids influence the activity of neuroendocrine dopaminergic neurons

DeMaria, Jamie E.; Livingstone, John D.; Freeman, Marc E.

doi:10.1016/s0006-8993(00)02763-3

Cited by 78 publications

(53 citation statements)

References 50 publications

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“…It was shown previously that administration of estrogen for a week decreased TH mRNA content in TIDA neurons and also lowered TH activity (23). On the other hand, the colocalization of CB1 receptors with dopaminergic pathways in other regions of the brain suggests functional interactions of DA with AEA in those regions similar to those in the hypothalamus (24).…”

Section: Discussionmentioning

confidence: 83%

The effect of anandamide on prolactin secretion is modulated by estrogen

Scorticati

Mohn

Laurentiis

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Recent research has revealed that endogenous cannabinoid receptors (CB1 and CB2) react with the active ingredient of marijuana, ⌬ 9 -tetrahydrocannabinol. Two endogenous ligands activate these receptors. The principal one, anandamide (AEA), activates CB1. AEA and CB1 are localized to various neurons within the brain. Because ⌬ 9 -tetrahydrocannabinol inhibited prolactin (Prl) secretion following its intraventricular injection into male rats, we hypothesized that AEA would have a similar effect. Estrogen modifies many hormonal responses and is known to increase Prl secretion. Therefore, we hypothesized that responses to intraventricular AEA would change depending on the gonadal steroid environment. Consequently, we evaluated the effects of lateral cerebral ventricular microinjection of AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed (OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect in OVX females, and increased Prl in OVX-E rats. The results were at least partially mediated by changes in dopaminergic turnover, altering the inhibitory dopaminergic control of Prl release by the anterior pituitary gland. Thus, dopamine turnover was increased in the male rats and decreased significantly in OVX and in OVX-E rats. The changes in Prl may be caused not only by altered dopamine input to the anterior pituitary gland but also by effects of AEA on other transmitters known to alter Prl release. Importantly, in OVX-E rats, the elevated Prl release and the response to AEA were blocked by the AEA antagonist, indicating that AEA is a synaptic transmitter released from neurons that decrease inhibitory control of Prl release.cannabinoid receptors ͉ estradiol ͉ dopamine ͉ CB1 antagonist ͉ dopamine receptors

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Section: Discussionmentioning

confidence: 83%

The effect of anandamide on prolactin secretion is modulated by estrogen

Scorticati

Mohn

Laurentiis

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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“…Several previous studies have examined the effects of sex steroids on prolactin gene expression and secretion and have found that these steroids exert their effects in association with dopamine. In a study of ovariectomized rats, both E2 and P4 negatively influenced the activity of neuroendocrine dopaminergic neurons and increased prolactin secretion [19]. E2 has also been shown to decrease the number of dopamine receptors in the anterior pituitary [20,21].…”

Section: Discussionmentioning

confidence: 99%

Effects of estradiol and progesterone on prolactin transcriptional activity in somatolactotrophic cells

et al. 2012

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THE SEX STEROIDS estradiol (E2) and progesterone (P4) regulate the synthesis and secretion of several pituitary hormones, and play a key role in the regulation of reproductive function. Lactotroph cells, which produce prolactin, are a known target of E2 action. Lactotrophs constitute approximately 15% of the cells of the adenohypophysis; however, this proportion is dependent on age and sex [1]. It has been reported that there is marked hyperplasia of lactotrophs during pregnancy and lactation in humans [2]. Exogenous E2 is known to induce lactotroph hyperplasia [3], and increases prolactin release from rat pituitary cultures by desensitizating lactotrophs to dopamine, a well-known inhibitor of prolactin release [4]. E2 was also reported Effects of estradiol and progesterone on prolactin transcriptional activity in somatolactotrophic cells Tselmeg Mijiddorj, Haruhiko Kanasaki, Indri Purwana, Sukhbaatar Unurjargal, Aki Oride and Kohji Miyazaki Department of Obstetrics and Gynecology, Shimane University School of Medicine, Izumo 693-8501, JapanAbstract. We examined the effects of sex steroids on prolactin promoter activity in rat somatolactotrophic GH3 cells. Both estradiol (E2) and progesterone (P4) were found to inhibit basal prolactin promoter activity, but to potentiate Thyrotropinreleasing hormone (TRH)-induced prolactin promoter activity. P4 had a greater inhibitory effect on basal prolactin promoter activity than E2, and P4 also potentiated TRH-induced prolactin promoter more potently than E2. Combined treatment with E2 and P4 further increased TRH-induced prolactin promoter activity. E2 and P4 also both reduced basal serum response element (SRE) promoter activity, and increased TRH-induced SRE promoter activity. Combination treatment with E2 and P4 reduced basal activity of SRE promoter and increased TRH-induced SRE activity more potently than E2 or P4 alone. In contrast, basal cAMP response element (CRE) promoter activity was not influenced by either E2 or P4, although TRHinduced CRE promoter was potentiated by each of these steroids, and was further increased by E2 and P4 combination treatment. Both E2 and P4 increased TRH-induced extracellular signal-regulated kinase (ERK) phosphorylation; however, intracellular cAMP levels was not influenced by E2 or P4. TRH-induced CRE promoter was inhibited by mitogen-activated protein kinase/ERK kinase (MEK) inhibitor and was increased by overexpression of MEK kinase (MEKK). This study showed that ERK and SRE transcriptional pathways, but not the cAMP/CRE pathway, may be involved in the suppression of basal prolactin promoter activity, whereas both the ERK/SRE and MAP kinase-mediated CRE pathways appear to be involved in the increased transcriptional efficiency of the prolactin promoter induced by TRH stimulation.Key words: Prolactin, Thyrotropin-releasing hormone (TRH), Estradiol, Progesterone, GH3 cells to stimulate lactotroph proliferation and prolactin gene expression in rats [5].E2 modulates gene expression through estrogen receptors (ERs), which belong to the n...

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“…Prolactin secretion increases with age, likely due to a reduction in hypothalamic dopamine activity, and a high incidence of prolactinomas is seen in old rats due to the lack of hypothalamic inhibitory control (Sarkar et al 1982, Stefaneanu & Kovacs 1994. In rats, estrogen is shown to stimulate prolactin release from lactotrophs and inhibited the activity of hypothalamic neuroendocrine dopaminergic neurons, and prolactinomas can be induced in rats by prolonged administration of estrogen (Welsch et al 1971, Sarkar et al 1982, Lloyd 1990, DeMaria et al 2000. Consequently, persistent changes in the androgenestrogen balance in the mixture groups may have played a role in the development of pituitary tumors.…”

Section: Reproductive Aging In Females and Pituitary Gland Changesmentioning

confidence: 99%

Late-life effects on rat reproductive system after developmental exposure to mixtures of endocrine disrupters

et al. 2014

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This study examined late-life effects of perinatal exposure of rats to a mixture of endocrine-disrupting contaminants. Four groups of 14 time-mated Wistar rats were exposed by gavage from gestation day 7 to pup day 22 to a mixture of 13 anti-androgenic and estrogenic chemicals including phthalates, pesticides, u.v.-filters, bisphenol A, parabens, and the drug paracetamol. The groups received vehicle (control), a mixture of all 13 chemicals at 150-times (TotalMix150) or 450-times (TotalMix450) high-end human exposure, or 450-times a mixture of nine predominantly anti-androgenic chemicals (AAMix450). Onset of puberty and estrous cyclicity at 9 and 12 months of age were assessed. Few female offspring showed significantly regular estrus cyclicity at 12 months of age in the TotalMix450 and AAMix450 groups compared with controls. In 19-month-old male offspring, epididymal sperm counts were lower than controls, and in ventral prostate an overrepresentation of findings related to hyperplasia was observed in exposed groups compared with controls, particularly in the group dosed with anti-androgens. A higher incidence of pituitary adenoma at 19 months of age was found in males and females in the AAMix450 group. Developmental exposure of rats to the highest dose of a human-relevant mixture of endocrine disrupters induced adverse effects late in life, manifested as earlier female reproductive senescence, reduced sperm counts, higher score for prostate atypical hyperplasia, and higher incidence of pituitary tumors. These delayed effects highlight the need for further studies on the role of endocrine disrupters in hormone-related disorders in aging humans.

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Ovarian steroids influence the activity of neuroendocrine dopaminergic neurons

Cited by 78 publications

References 50 publications

The effect of anandamide on prolactin secretion is modulated by estrogen

The effect of anandamide on prolactin secretion is modulated by estrogen

Effects of estradiol and progesterone on prolactin transcriptional activity in somatolactotrophic cells

Late-life effects on rat reproductive system after developmental exposure to mixtures of endocrine disrupters

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