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hyperprolactinemia/tyrosine
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Tyrosine hydroxylase and POMC mRNA in the arcuate region are increased by castration and hyperprolactinemia.
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We have examined the changes which occur in neuronal expression of tyrosine hydroxylase (TH) and proopiomelanocortin (POMC) mRNA in response to castration and hyperprolactinemia (HP) in male rats. Steady-state mRNA levels were determined by quantitative in situ hybridization histochemistry (ISHH)
Hyperprolactinemia increases and hypoprolactinemia decreases tyrosine hydroxylase messenger ribonucleic acid levels in the arcuate nuclei, but not the substantia nigra or zona incerta.
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The effects of experimentally produced hypoprolactinemia and hyperprolactinemia on tyrosine hydroxylase (TH) mRNA signal levels were examined in dopaminergic neurons ovariectomized rats. TH mRNA signal levels and relative TH quantity in the arcuate nuclei, zona incerta, and substantia nigra were
Mass and in situ activity of tyrosine hydroxylase in the median eminence: effect of hyperprolactinemia.
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The role of PRL in the control of catecholaminergic hypothalamic neurons of female rats was investigated. The in situ activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in the median eminence
Prolactin and TSH response to alpha-methyl-l-tyrosine in normal subjects and in women with pathological hyperprolactinemia.
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Effects of ovariectomy and hyperprolactinemia on tyrosine hydroxylase and dopamine-beta-hydroxylase activity in various limbic and hypothalamic structures.
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Expanding phenotype and clinical analysis of tyrosine hydroxylase deficiency.
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This study included 12 Chinese patients with a wide spectrum of phenotypes of tyrosine hydroxylase deficiency. Seven females and 5 males, aged 2.2 to 41 years, had phenotypes ranging from severe type with onset at infancy to mild type with onset after 3 years of age. Patients with the severe type
Modulation of stress-induced and stimulated hyperprolactinemia with the group II metabotropic glutamate receptor selective agonist, LY379268.
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It is well recognized that glutamate is an integral excitatory neurotransmitter in the neuroendocrine control of several hormonal factors. While the ability of pharmacological agents acting at ionotropic glutamate receptors to modulate the levels of serum prolactin levels has been investigated,
Hyperprolactinaemia and DNA synthesis in the pituitary gland of the rat.
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Hyperprolactinaemia produced in rats by the transplanted prolactin-secreting tumours MtTW15 and 7315a significantly (P less than 0.01) inhibited by 70% the incorporation of [3H]thymidine into the pituitary DNA of the host animals. The weight and the DNA content of the glands were significantly (P
The central mechanism of risperidone-induced hyperprolactinemia.
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Risperidone is known to increase prolactin secretion in treating mental illness patients. This side-effect is thought to be mediated via central signaling pathway. However, the exact pathway involved between risperidone and hyperprolactinemia are still unknown. Therefore, we have treated mice with
Hyperiodotyrosinemia-induced hyperprolactinemia and hyperaldosteronism.
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A 21-year-old goitrous hypothyroid Chinese woman had elevated serum iodotyrosines with a monoiodotyrosine level of 85.9 nmol/l (normal 0.49-0.89 nmol/l) and a diiodotyrosine level of 25.3 nmol/l (normal 0.023-0.53 nmol/l). She was amenorrheic with low luteinizing hormone and follicle-stimulating
Catecholamine utilization in specific rat brain nuclei after short-term hyperprolactinaemia.
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Endogenous hyperprolactinaemia was induced in intact male rats by transplantation of pituitaries under the kidney capsule. Five days later the utilization of noradrenaline (NA) and dopamine (DA) in individual brain nuclei and changes of plasma prolaction (PRL) were measured. Inhibition of
Glial cell line-derived neurotrophic factor gene therapy ameliorates chronic hyperprolactinemia in senile rats.
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Progressive dysfunction of hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons during normal aging is associated in the female rat with chronic hyperprolactinemia. We assessed the effectiveness of glial cell line-derived neurotrophic factor (GDNF) gene therapy to restore TIDA neuron function
Prolactin and thyrotropin response to blockade of dopamine synthesis by monoiodotyrosine in subjects with postpartum and pathological hyperprolactinemia.
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To better understand the state of dopamine (DA) neurotransmission in the tuberoinfundibular DA system (TIDA), monoiodotyrosine (3-iodo-L-tyrosine, MIT), a potent inhibitor of DA synthesis, was acutely administered to 8 normal women, 7 postpartum women, 8 women with pathological hyperprolactinemia
Catecholamines and pituitary function. IV. Effects of low-dose dopamine infusion and long-term bromocriptine treatment on the abnormal thyrotroph (TSH) dynamics in patients with pathological hyperprolactinaemia.
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In order to gain further insight into the role of dopamine (DA) in the control of TSH release and to investigate whether an increased or defective DA inhibition on pituitary thyrotrophs may be considered responsible for the abnormal TSH dynamics in pathological hyperprolactinaemia, we examined the
Changes in the catecholamine metabolism in the adrenal medulla of male hamsters with experimental hyperprolactinemia.
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1. Prolactin (PRL) can play a role as a physiological modulator of adrenal medulla function in several rodents. 2. We have examined the effects of hyperprolactinemia induced by ectopic pituitary grafts in Syrian hamsters on the adrenal medulla contents of catecholamines (CA) and their metabolites,
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