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Neurochemical evidence that estrogen-induced suppression of kappa-opioid-receptor-mediated regulation of tuberoinfundibular dopaminergic neurons is prolactin-independent. 1994

E J Wagner, and J Manzanares, and K E Moore, and K J Lookingland
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824.

The purpose of the present study was to examine the role of estrogen and prolactin in determining the responsiveness of tuberoinfundibular dopaminergic (TIDA) neurons to kappa-opioid receptor blockade in female rats. TIDA neuronal activity was estimated by measuring either dopamine synthesis [accumulation of 3,4-dihydroxyphenylalanine (DOPA) 30 min after the administration of the decarboxylase inhibitor NSD-1015] or metabolism [concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC)] in terminals of these neurons in the median eminence. Blockade of kappa-opioid receptors with the selective kappa-antagonist norbinaltorphimine (NOR-BNI) increased the concentrations of DOPAC in the median eminence of ovariectomized rats but had no effect in gonadally intact rats, suggesting that loss of endogenous ovarian hormones following ovariectomy results in an increase in kappa-opioid-receptor-mediated inhibition of TIDA neurons. Estrogen administration ot ovariectomized rats blocked NOR-BNI-induced increases in median eminence DOPAC concentrations, whereas treatment of gonadally intact or ovariectomized, estrogen-treated rats with prolactin antiserum had no effect on the insensitivity of these neurons to NOR-BNI. Administration of antiserum to dynorphin A1-8 increased DOPA accumulation in the median eminence of ovariectomized but not estrogen-treated ovariectomized rats. Taken together, these results reveal that estrogen, acting via a prolactin-independent mechanism, suppresses kappa-opioid-receptor-mediated inhibition of the activity of TIDA neurons, possibly by decreasing the release of endogenous dynorphin.

UI MeSH Term Description Entries
D007028 Hypothalamic Hormones Peptide hormones produced by NEURONS of various regions in the HYPOTHALAMUS. They are released into the pituitary portal circulation to stimulate or inhibit PITUITARY GLAND functions. VASOPRESSIN and OXYTOCIN, though produced in the hypothalamus, are not included here for they are transported down the AXONS to the POSTERIOR LOBE OF PITUITARY before being released into the portal circulation. Hypothalamic Pituitary-Regulating Hormones,Hypothalamic Pituitary-Regulating Peptides,Hormones, Hypothalamic,Hormones, Hypothalamic Pituitary-Regulating,Hypothalamic Pituitary Regulating Hormones,Hypothalamic Pituitary Regulating Peptides,Peptides, Hypothalamic Pituitary-Regulating,Pituitary-Regulating Hormones, Hypothalamic,Pituitary-Regulating Peptides, Hypothalamic
D007276 Injections, Intraventricular Injections into the cerebral ventricles. Intraventricular Injections,Injection, Intraventricular,Intraventricular Injection
D008473 Median Eminence Raised area at the infundibular region of the HYPOTHALAMUS at the floor of the BRAIN, ventral to the THIRD VENTRICLE and adjacent to the ARCUATE NUCLEUS OF HYPOTHALAMUS. It contains the terminals of hypothalamic neurons and the capillary network of hypophyseal portal system, thus serving as a neuroendocrine link between the brain and the PITUITARY GLAND. Eminentia Mediana,Medial Eminence,Eminence, Medial,Eminence, Median,Eminences, Medial,Eminentia Medianas,Medial Eminences,Mediana, Eminentia,Medianas, Eminentia
D009271 Naltrexone Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence. Antaxone,Celupan,EN-1639A,Nalorex,Naltrexone Hydrochloride,Nemexin,ReVia,Trexan,EN 1639A,EN1639A
D009411 Nerve Endings Branch-like terminations of NERVE FIBERS, sensory or motor NEURONS. Endings of sensory neurons are the beginnings of afferent pathway to the CENTRAL NERVOUS SYSTEM. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called PRESYNAPTIC TERMINALS. Ending, Nerve,Endings, Nerve,Nerve Ending
D009474 Neurons The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM. Nerve Cells,Cell, Nerve,Cells, Nerve,Nerve Cell,Neuron
D010052 Ovariectomy The surgical removal of one or both ovaries. Castration, Female,Oophorectomy,Bilateral Ovariectomy,Bilateral Ovariectomies,Castrations, Female,Female Castration,Female Castrations,Oophorectomies,Ovariectomies,Ovariectomies, Bilateral,Ovariectomy, Bilateral
D010446 Peptide Fragments Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques. Peptide Fragment,Fragment, Peptide,Fragments, Peptide
D011388 Prolactin A lactogenic hormone secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). It is a polypeptide of approximately 23 kD. Besides its major action on lactation, in some species prolactin exerts effects on reproduction, maternal behavior, fat metabolism, immunomodulation and osmoregulation. Prolactin receptors are present in the mammary gland, hypothalamus, liver, ovary, testis, and prostate. Lactogenic Hormone, Pituitary,Mammotropic Hormone, Pituitary,Mammotropin,PRL (Prolactin),Hormone, Pituitary Lactogenic,Hormone, Pituitary Mammotropic,Pituitary Lactogenic Hormone,Pituitary Mammotropic Hormone
D001923 Brain Chemistry Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states. Chemistry, Brain,Brain Chemistries,Chemistries, Brain

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