Dopamine as a prolactin (PRL) inhibitor.
Nira Ben-Jonathan,Robert Hnasko +1 more
TL;DR: PRL homeostasis should be viewed in the context of a fine balance between the action of dopamine as an inhibitor and the many hypothalamic, systemic, and local factors acting as stimulators, none of which has yet emerged as a primary PRL releasing factor.
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Abstract: Dopamine is a small and relatively simple molecule that fulfills diverse functions. Within the brain, it acts as a classical neurotransmitter whose attenuation or overactivity can result in disorders such as Parkinson’s disease and schizophrenia. Major advances in the cloning and characterization of biosynthetic enzymes, transporters, and receptors have increased our knowledge regarding the metabolism, release, reuptake, and mechanism of action of dopamine. Dopamine reaches the pituitary via hypophysial portal blood from several hypothalamic nerve tracts that are regulated by PRL itself, estrogens, and several neuropeptides and neurotransmitters. Dopamine binds to type-2 dopamine receptors that are functionally linked to membrane channels and G proteins and suppresses the high intrinsic secretory activity of the pituitary lactotrophs. In addition to inhibiting PRL release by controlling calcium fluxes, dopamine activates several interacting intracellular signaling pathways and suppresses PRL gene expression and lactotroph proliferation. Thus, PRL homeostasis should be viewed in the context of a fine balance between the action of dopamine as an inhibitor and the many hypothalamic, systemic, and local factors acting as stimulators, none of which has yet emerged as a primary PRL releasing factor. The generation of transgenic animals with overexpressed or mutated genes expanded our understanding of dopamine-PRL interactions and the physiological consequences of their perturbations. PRL release in humans, which differs in many respects from that in laboratory animals, is affected by several drugs used in clinical practice. Hyperprolactinemia is a major neuroendocrine-related cause of reproductive disturbances in both men and women. The treatment of hyperprolactinemia has greatly benefited from the generation of progressively more effective and selective dopaminergic drugs. (Endocrine Reviews 22: 724–763, 2001)
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The role of dopamine in the pathophysiology of depression.
TL;DR: Several studies support the hypothesis that major depression is associated with a state of reduced DA transmission, possibly reflected bycompensatory up-regulation of D2receptors, and further research on the contribution of DA to the pathophysiology of depression is justified to improve outcomes for patients with treatment-resistant and nonremitting depression.
Physical Health Monitoring of Patients With Schizophrenia
Stephen R. Marder,Susan M. Essock,Alexander L. Miller,Robert W. Buchanan,Daniel E. Casey,John M. Davis,John M. Kane,Jeffrey A. Lieberman,Nina R. Schooler,Nancy H. Covell,Scott Stroup,Ellen M. Weissman,Donna A. Wirshing,Catherine S. Hall,Leonard M. Pogach,Xavier Pi-Sunyer,J. Thomas Bigger,Alan W. Friedman,David L. Kleinberg,Steven J. Yevich,Bonnie M. Davis,Steven S. Shon +21 more
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Enkephalin inhibits dopamine synthesis in vitro in the median eminence portion of rat hypothalamic slices.
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TL;DR: Tyrosine hydroxylase mRNA was visualized in the whole brain from 13 days of gestation, but the largest increase of the expression was observed in the hypothalamus, and the relative gene expressions of the three enzymes involved in the biosynthesis of catecholamines and phenolamines in nervous tissues were discussed.
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A growth hormone/prolactin-binding protein in human milk
Moisés Mercado,Gerhard Baumann +1 more
TL;DR: It is concluded that human milk contains a high affinity GH/PRLBP that differs from the serum GHBP in its ligand specificity, molecular size, immunological, and glycosylation characteristics.
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Prolactin gene disruption does not compromise differentiation of tuberoinfundibular dopaminergic neurons.
TL;DR: Assessment of hypophysiotropic tuberoinfundibular dopaminergic neurons in mice with spontaneous mutations in transcription factors Prop-1 or Pit-1 suggests that, although absence of the stimulatory PRL feedback signal results in diminished activity of TIDA neurons, differentiation of these cells is not adversely affected.
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