Catecholamines in hypothalamus, ovaries and uteri of rats with precocious puberty

Pantić, V.; Demajo, Miroslav; Loncar-Stevanović, H

doi:10.1007/bf03348923

Cited by 8 publications

(4 citation statements)

References 27 publications

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“…These alterations in the CPP subjects suggested an up-regulated catecholamine metabolic pathway (Fig. 4A) and enhanced sympathetic nervous system activity, which are in agreement with previous observations of increased noradrenaline and adrenaline levels in both the ovaries and uteri of precocious female rats induced by hypothalamic lesions (42).…”

Section: Urinary Metabolites From Triptorelin and Derivatives-trip-supporting

confidence: 92%

Urinary Metabolite Markers of Precocious Puberty

Пин

Zhang

et al. 2012

Molecular & Cellular Proteomics

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The incidence of precocious puberty (PP, the appearance of signs of pubertal development at an abnormally early age), is rapidly rising, concurrent with changes of diet, lifestyles, and social environment. The current diagnostic methods are based on a hormone (gonadotropin-releasing hormone) stimulation test, which is costly, time-consuming, and uncomfortable for patients. The lack of molecular biomarkers to support simple laboratory tests, such as a blood or urine test, has been a long standing bottleneck in the clinical diagnosis and evaluation of PP. Here we report a metabolomic study using an ultra performance liquid chromatography-quadrupole time of flight mass spectrometry and gas chromatography-time of flight mass spectrometry. Urine metabolites from 163 individuals were profiled, and the metabolic alterations were analyzed after treatment of central precocious puberty (CPP) with triptorelin depot. A panel of biomarkers selected from >70 differentially expressed urinary metabolites by receiver operating characteristic and logistic regression analysis provided excellent predictive power with high sensitivity and specificity for PP. The altered metabolic profile of the PP patients was characterized by three major perturbed metabolic pathways: catecholamine, serotonin metabolism, and tricarboxylic acid cycle, presumably resulting from activation of the sympathetic nervous system and the hypothalamic-pituitary-gonadal axis. Treatment with triptorelin depot was able to normalize these three altered pathways. Additionally, significant changes in the urine levels of 4-hydroxyphenylacetic acid, 5-hydroxyindoleacetic acid, indoleacetic acid, 5-hydroxytryptophan, and 5-hydroxykynurenamine in the CPP group suggest that the development of CPP condi-

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Section: Urinary Metabolites From Triptorelin and Derivatives-trip-supporting

confidence: 92%

Urinary Metabolite Markers of Precocious Puberty

Пин

Zhang

et al. 2012

Molecular & Cellular Proteomics

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“…The noradrenergic innervation of the ovary acts tonically inhibitory during the selection of follicles triggered for the process of development and ripening (1,6,12). The decreased NE concentrations in the hyperluteinized ovaries as compared to those of intact controls as demonstrated previously (19), may explain the increased ovarian MAO activity in the hyperluteinized ovaries.…”

Section: Discussionmentioning

confidence: 57%

Total monoamine oxidase activity in the hypothalamus, ovary and uterus of rats with an extreme number of ovarian corpora lutea

Demajo¹,

Petrović²,

Cvijic̀³

2003

Acta Physiologica Hungarica

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The activity of total monoamine oxidase (MAO) in the rat ovary and uterus fluctuates significantly under various physiological conditions. We analyzed total MAO activity in the hypothalamus, uterus and ovary in adult rats, having an extreme number of corpora lutea (hyperluteinized ovaries) resulting from the mechanical lesions in the posterior hypothalamic region of neonatal rats. Total MAO activity in the hypothalamus (30.21 +/- 1.53 pmol/mg tissue/min) and uterus (3.16 +/- 0.61 pmol/mg tissue/min) of rats with hyperluteinized ovaries did not show a significant difference as compared to that of intact controls (31.09 +/- 1.72 and 2.90 +/- 0.40 pmol/mg tissue/min, respectively). In contrast, in the ovaries of hyperluteinized rats, total MAO activity (21.16 +/- 1.70 pmol/mg tissue/min) was significantly higher (p<0.01) when compared to that of intact controls (13.61 +/- 1.30 pmol/mg tissue/min). The increased MAO activity in the hyperluteinized ovaries may be attributed to the increased number of transformed and accumulated corpora lutes as a consequence of diminished luteolysis.

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“…The discrepancy may be due to differences in methods and sampling locations. Nonetheless, hypothalamic concentrations of NE in female rats with posterior hypothalamic lesions exhibiting precocious puberty and in control rats on the day of vaginal opening are higher than in prepubertal control rats (451), and NE turnover rates in the MPOA increase when estrogen induces an LH surge in P15 female rats (452), similar to those observed with the proestrous surge, indicating that NE may be involved in the first LHRH surge, and hence the onset of puberty in rats (453).…”

Section: The Catecholamine Norepinephrine (Ne)mentioning

confidence: 77%

Neurobiological Mechanisms of the Onset of Puberty in Primates*

2001

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An increase in pulsatile release of LHRH is essential for the onset of puberty. However, the mechanism controlling the pubertal increase in LHRH release is still unclear. In primates the LHRH neurosecretory system is already active during the neonatal period but subsequently enters a dormant state in the juvenile/prepubertal period. Neither gonadal steroid hormones nor the absence of facilitatory neuronal inputs to LHRH neurons is responsible for the low levels of LHRH release before the onset of puberty in primates. Recent studies suggest that during the prepubertal period an inhibitory neuronal system suppresses LHRH release and that during the subsequent maturation of the hypothalamus this prepubertal inhibition is removed, allowing the adult pattern of pulsatile LHRH release. In fact, y-aminobutyric acid (GABA) appears to be an inhibitory neurotransmitter responsible for restricting LHRH release before the onset of puberty in female rhesus monkeys. In addition, it appears that the reduction in tonic GABA inhibition allows an increase in the release of glutamate as well as other neurotransmitters, which contributes to the increase in pubertal LHRH release. In this review, developmental changes in several neurotransmitter systems controlling pulsatile LHRH release are extensively reviewed.

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Catecholamines in hypothalamus, ovaries and uteri of rats with precocious puberty

Cited by 8 publications

References 27 publications

Urinary Metabolite Markers of Precocious Puberty

Urinary Metabolite Markers of Precocious Puberty

Total monoamine oxidase activity in the hypothalamus, ovary and uterus of rats with an extreme number of ovarian corpora lutea

Neurobiological Mechanisms of the Onset of Puberty in Primates*

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