Relevant bibliographies by topics / Dopaminergic mechanisms. Estrogen. Prolactin

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Academic literature on the topic 'Dopaminergic mechanisms. Estrogen. Prolactin'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Dopaminergic mechanisms. Estrogen. Prolactin"

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Grattan, David R., Christine L. Jasoni, Xinhuai Liu, Greg M. Anderson, and Allan E. Herbison. "Prolactin Regulation of Gonadotropin-Releasing Hormone Neurons to Suppress Luteinizing Hormone Secretion in Mice." Endocrinology 148, no. 9 (2007): 4344–51. http://dx.doi.org/10.1210/en.2007-0403.

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Hyperprolactinemia causes infertility, but the mechanisms involved are not known. The present study aimed to determine whether and how prolactin may influence LH secretion in the adult female mouse. Using ovariectomized, estrogen-treated (OVX+E) mice, we found that 7 d of intracerebroventricular prolactin potently suppressed serum LH levels (P < 0.05). To examine whether this central action of prolactin may involve the GnRH neurons, the effects of acute and chronic prolactin on cAMP response element-binding protein phosphorylation (pCREB) in GnRH neurons were examined using dual-label i
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MohanKumar, Sheba M. J., Badrinarayanan S. Kasturi, Andrew C. Shin, et al. "Chronic estradiol exposure induces oxidative stress in the hypothalamus to decrease hypothalamic dopamine and cause hyperprolactinemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 3 (2011): R693—R699. http://dx.doi.org/10.1152/ajpregu.00481.2010.

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Estrogens are known to cause hyperprolactinemia, most probably by acting on the tuberoinfundibular dopaminergic (TIDA) system of the hypothalamus. Dopamine (DA) produced by TIDA neurons directly inhibits prolactin secretion and, therefore, to stimulate prolactin secretion, estrogens inhibit TIDA neurons to decrease DA production. However, the mechanism by which estrogen produces this effect is not clear. In the present study, we used a paradigm involving chronic exposure to low levels of estradiol-17β (E2) to mimic prolonged exposures to environmental and endogenous estrogens. We hypothesized
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Gunin, AG, V. Emelianov, AS Tolmachev, and A. Tolmacheva. "Effect of prolactin and dopaminergic drugs on uterine response to chronic estrogen exposure." Journal of Endocrinology 172, no. 1 (2002): 61–69. http://dx.doi.org/10.1677/joe.0.1720061.

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The aim of this work was to examine the role of prolactin and dopaminergic drugs, which affect prolactin secretion, on proliferative and morphogenetic reactions in the uterus under continuous estrogen treatment. Ovariectomized mice received injections of estradiol dipropionate (2 microg per 100 g, weekly) or vehicle and daily injections of prolactin (0.25 mg/100 g) or saline (0.05 ml) for 30 days. Other groups of mice received injections of estradiol or vehicle and injections of saline, and were allowed to drink bromocriptine (25 mg/l), metoclopramide (25 mg/l), or only tap water for 30 days.
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Piccini, Paola, Angelo Nuti, Anna Maria Paoletti, Alessandro Napolitano, Gian Benedetto Melis, and Ubaldo Bonuccelli. "Possible Involvement of Dopaminergic Mechanisms in the Antimigraine Action of Flunarizine." Cephalalgia 10, no. 1 (1990): 3–8. http://dx.doi.org/10.1046/j.1468-2982.1990.1001003.x.

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Flunarizine, a calcium antagonist widely used in the prophylactic treatment of migraine, may interfere with dopaminergic systems. Flunarizine therapy can in fact induce extrapyramidal side effects and can increase basal as well as stimulated prolactin levels. To better define the mechanism of flunarizine action in migraine, we studied prolactin and growth hormone responses to thyrotropin releasing hormone and sulpiride in 13 female migraineurs before and after 60 days of flunarizine therapy. The treatment did not modify basal prolactin and growth hormone levels, but prolactin response to thyro
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Yuan, Zung Fan, Shu-Chuan Yang, and Jenn-Tser Pan. "Effects of prolactin-releasing peptide on tuberoinfundibular dopaminergic neuronal activity and prolactin secretion in estrogen-treated female rats." Journal of Biomedical Science 9, no. 2 (2002): 112–18. http://dx.doi.org/10.1007/bf02256021.

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Shieh, Kun-Ruey, and Jenn-Tser Pan. "Effects of orphanin FQ on central dopaminergic neuronal activities and prolactin secretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 3 (2001): R705—R712. http://dx.doi.org/10.1152/ajpregu.2001.280.3.r705.

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Effects of orphanin FQ (OFQ) on central dopaminergic (DA) neurons and serum prolactin (PRL) were examined in ovariectomized, estrogen-primed Sprague-Dawley rats. The activities of central DA neurons, including the tuberoinfundibular (TI), nigrostriatal, mesolimbic, and incertohypothalamic ones, were determined by measuring the levels of 3,4-dihydroxyphenylacetic acid (DOPAC), the major metabolite of dopamine, in their projection regions in the brain by HPLC plus electrochemical detection. Intracerebroventricular administration of OFQ lowered DOPAC levels in the median eminence (ME), striatum,
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Hou, Yueping, Shu-Ping Yang та James L. Voogt. "Changes in Estrogen Receptor-α Expression in Hypothalamic Dopaminergic Neurons During Proestrous Prolactin Surge". Endocrine 20, № 1-2 (2003): 131–38. http://dx.doi.org/10.1385/endo:20:1-2:131.

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Veselinović, Tanja, Holger Schorn, Ingo B. Vernaleken, Katharina Schiffl, Majken Klomp, and Gerhard Gründer. "Impact of Different Antidopaminergic Mechanisms on the Dopaminergic Control of Prolactin Secretion." Journal of Clinical Psychopharmacology 31, no. 2 (2011): 214–20. http://dx.doi.org/10.1097/jcp.0b013e31820e4832.

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Cristina, C., G. Díaz-Torga, A. Baldi, et al. "Increased Pituitary Vascular Endothelial Growth Factor-A in Dopaminergic D2 Receptor Knockout Female Mice." Endocrinology 146, no. 7 (2005): 2952–62. http://dx.doi.org/10.1210/en.2004-1445.

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Abstract Vascular endothelial growth factor (VEGF)-A is an important angiogenic cytokine in cancer and pathological angiogenesis and has been related to the antiangiogenic activity of dopamine in endothelial cells. We investigated VEGF expression, localization, and function in pituitary hyperplasia of dopamine D2 receptor (D2R)-knockout female mice. Pituitaries from knockout mice showed increased protein and mRNA VEGF-A expression when compared with wild-type mice. In wild-type mice, prolonged treatment with the D2R antagonist, haloperidol, enhanced pituitary VEGF expression and prolactin rele
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El-Azouzi, Mustapha, Dora W. Hsu, Peter McL Black, et al. "The importance of dopamine in the pathogenesis of experimental prolactinomas." Journal of Neurosurgery 72, no. 2 (1990): 273–81. http://dx.doi.org/10.3171/jns.1990.72.2.0273.

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✓ The factors responsible for the production of prolactin-secreting tumors are obscure. One hypothesis, that chronic loss of dopamine control from the hypothalamus may be associated with prolactinoma formation, was tested. Female adult Fischer 344 rats were subjected to ovariectomy and were then given subcutaneous implants of diethylstilbestrol (DES) Silastic capsules to produce lactotrophic hyperplasia. Sequential studies assessed the neuronal activity of the tuberoinfundibular dopaminergic neurons of the arcuate nucleus of the hypothalamus (A12) during and after this estrogen-induced pituita
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Dissertations / Theses on the topic "Dopaminergic mechanisms. Estrogen. Prolactin"

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Johnson, Brandi Nicole. "Dopaminergic mechanisms involved in estrogen modulation of the prolactin response to Orphanin FQ/Nociceptin." Oxford, Ohio : Miami University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=miami1152115599.

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LaPensee, Elizabeth W. "Mechanisms of Chemoresistance in Breast Cancer and Liposarcoma." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1224593025.

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Yuan, Zung Fan, and 袁宗凡. "Effects of Prolactin-Releasing Factors on the Afternoon Prolactin Surge and the Tuberoinfundibular Dopaminergic Neuronal Activity in Ovariectomized, Estrogen-Treated Rats." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/90903035250966515887.

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博士<br>國立陽明大學<br>生理學研究所<br>90<br>The secretion of prolactin (PRL) is mainly regulated by the inhibitory input from the hypothalamus and dopamine (DA) is the well-accepted PRL-inhibitory hormone. Nevertheless, its secretion is also stimulated by a group of putative PRL-releasing factors (PRFs), e.g., thyrotropin-releasing hormone (TRH), oxytocin, vasopressin, vasoactive intestinal peptide, angiotensin II (AII), a newly discovered prolactin-releasing peptide (PrRP), etc. None of them, however, fulfills all criteria of a hypothalamic releasing hormone. In this thesis, the roles of AII, TRH and PrR
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Yen, Shih-Hui, and 顏世慧. "The Action Mechanisms of Progesterone on Tuberoinfundibular Dopaminergic Neuronal Activity and Prolactin Secretion." Thesis, 1998. http://ndltd.ncl.edu.tw/handle/15023197216882911804.

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博士<br>國立陽明大學<br>生理學研究所<br>87<br>The ovary is the major site for synthesis and secretion of progesterone (P4) in mammals. The major physiological functions of P4 include: control of ovulation, facilitation of implantation, and maintenance of pregnancy by promoting uterine growth and suppressing myometrial contractility. A diurnal change of tuberoinfundibular dopaminergic (TIDA) neuronal activity exists in female rats, which is prerequisite for the estrogen-induced afternoon PRL-surge. In adult ovariectomized (OVX) and estrogen (E2)-primed Sprague-Dawley rats, P4 (2 mg/kg sc, given at
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YANG, JIANN-YUEH, and 楊健岳. "Effect of thyroidectomy on prolactin secretion in ovariectomized, estrogen-treated rats: the role of the tuberoinfundibular dopaminergic." Thesis, 1992. http://ndltd.ncl.edu.tw/handle/71374473335590437395.

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Book chapters on the topic "Dopaminergic mechanisms. Estrogen. Prolactin"

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Albert, Paul R., Mohammad H. Ghahremani, and Stephen J. Morris. "Mechanisms of Dopaminergic Regulation of Prolactin Secretion." In The Dopamine Receptors. Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2635-0_12.

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Hruska, R. E. "Differentiation of Postsynaptic Dopamine Receptor Density Altered by Estrogen and the Modulatory Role of Prolactin." In Dopaminergic Systems and their Regulation. Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_25.

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Clopton, J. K., and J. H. Gordon. "Separate Molecular Mechanisms for Estrogen-induced Up- and Down-regulation of Striatal Dopamine Receptors." In Dopaminergic Systems and their Regulation. Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_20.

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Shull, James D., and Jack Gorski. "The Hormonal Regulation of Prolactin Gene Expression: An Examination of Mechanisms Controlling Prolactin Synthesis and the Possible Relationship of Estrogen to These Mechanisms." In Vitamins & Hormones. Elsevier, 1986. http://dx.doi.org/10.1016/s0083-6729(08)60421-5.

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Kayabekir, Murat. "Neurophysiology of Basic Molecules Affecting Sleep and Wakefulness Mechanisms, Fundamentals of Sleep Pharmacology." In Sleep Medicine and the Evolution of Contemporary Sleep Pharmacotherapy [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100166.

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As part of the biological rhythm, the human brain has a healthy functioning with the ability to differentiate between day and night hours in any given day (sleep rhythm, life rhythm). From the control of hormone levels to muscle tonus, from the regulation of respiratory rate to the content of our thoughts, sleep has an impact on all bodily and cognitive functions. It is not surprising to see such effects of sleep on the body as it leads to significant changes in the electrical activity of the brain in general. Electrical signal changes in the brain (sleep-wakefulness rhythm) are regulated by neurohormonal molecules and their receptors in the body. Neurotransmitters that control sleep and wakefulness can be listed as “Glutamate, Acetylcholine, Histamine, Norepinephrine and GABA”. Main hormones are: Melatonin, Corticotropin Releasing Hormone (CRH), cortisol, prolactin, Growth Hormone (GH), Insulin like Growth Factor (IGF-1, Somatomedin-C), Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH), progesterone, estrogen, testosterone, catecholamines, leptin and neuropeptide Y″. The effects of pharmacological agents on sleep and wakefulness cycles are materialized through the following molecules and their receptors: Hypnotics (GABA A agonists, benzodiazepines, gabapentin, tiagabine), sedative antidepressants (tricyclic antidepressants, trazadone, mitrazapine), antihistamines, medications used for the treatment of sleeplessness (melatonin and melatonin analogues), amphetamine (most commonly used stimulant), secretion of monoamines (dopamine), non-amphetamine stimulants used in the treatment of hypersomnia and narcolepsy (modafinil, bupropion, selegiline, caffeine) and other substances (alcohol, nicotine, anesthetics). To the extent we can conceptualize the physiological mechanisms of these basic molecules listed above and the regions they affect, we can appreciate the effects of these substances on sleep physiology and sleep disorders.
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