Effect of manipulating central catecholamines on puberty and the surge of luteinizing hormone and gonadotropin releasing hormone induced by pregnant mare serum gonadotropin in female rats.
Abstract: We have investigated the effect of manipulating central catecholamines on the timing of puberty (as assessed by vaginal opening) in female rats and the surge of luteinizing hormone (LH) and gonadotropin releasing hormone (GnRH) induced by pregnant mare serum gonadotropin (PMSG) in immature female rats. Manipulation of the catecholamines was carried out with either 6-hydroxydopamine (6-OHDA) administered with or without either desipramine (DMI) or pargyline, or alpha-methyl-p-tyrosine (alpha-MPT). The neonatal administration of 6-OHDA delayed puberty, an effect which was potentiated by pretreatment with DMI and was associated with a reduction in the rate of body growth. Catecholamine fluorescence in animals aged 60--65 days that had been treated with DMI followed by 6-OHDA was diminished only in the caudatus--putamen; treatment with 6-OHDA alone resulted in diminished fluorescence in the hypothalamus and in the intermediate but not the external layer of the median eminence. The neonatal administration of alpha-MPT had no significant effect on either the growth rate or the timing of puberty. Regular oestrous cycle occurred after puberty in animals treated with either 6-OHDA or alpha-MPT. The PMSG-induced LH surge was significantly enhanced by 6-OHDA (administered i.v.) plus DMI, and reduced by 6-OHDA injected in to the lateral ventricle (v). The inhibitory effect of 6-OHDA (v) was reduced by DMI, but in animals given 6-OHDA (i.v.) after pargyline there was a marked reduction in the height of the LH surge. There was a good correlation between the changes in the concentrations of LH in peripheral plasma and the concentrations of GnRH in pituitary stalk plasma in that the PMSG-induced surge of GnRH was significantly increased by 6-OHDA (i.v.) plus DMI and reduced by 6-OHDA (v). In animals treated with 6-OHDA (i.v. plus DMI catecholamine fluorescence was reduced only in the external layer of the median eminence, while after 6-OHDA (v) plus DMI degeneration was seen in the medial forebrain bundle. These results demonstrate a marked difference between the long-term and acute effects of 6-OHDA on the gonadotropin control system. Neonatal treatment with 6-OHDA plus DMI significantly delays puberty and the rate of body growth, but does not affect cyclical gonadotropin release and has no persistent effect on the hypothalamic catecholaminergic systems. The acute administration of 6-OHDA, depending upon the route of administration and whether it is given after DMI, can either potentiate or inhibit the PMSG-induced surge of GnRH and consequently LH by mechanisms which involve destruction, respectively, of either dopaminergic terminals in the median eminence or catecholaminergic fibres in the dorsal hypothalamus.
Publication Date: 1981-06-01 PubMed ID: 6113874DOI: 10.1016/0006-8993(81)90239-0Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The research article explores the impact of manipulating catecholamines, neurochemicals in the brain, on the onset of puberty and hormone surges in female rats. Specifically, it looks at the effect of treatments involving a neurotoxin and two other chemicals on hormone production and body growth.
Research Objectives and Methodology
- The researchers primary intention was to study how altering the levels of catecholamines, a type of neurotransmitter or brain chemical, could affect puberty and hormone release in female rats. They were particularly interested in the hormones luteinizing hormone (LH) and gonadotropin releasing hormone (GnRH), which help regulate the female reproductive cycle.
- The catecholamines were manipulated using different chemicals: the neurotoxin 6-hydroxydopamine (6-OHDA), desipramine (DMI), pargyline, or alpha-methyl-p-tyrosine (alpha-MPT).
- Apart from hormone production, the researchers also studied how these treatments affected the rats’ rate of body growth and the physical development of reproductive structures (vaginal opening).
Key Findings
- The researchers found that administering 6-OHDA to the rats postponed their onset of puberty and slowed their growth rate. This effect was intensified when DMI was also used.
- Treatments involving 6-OHDA affected different brain regions, leading to diminished catecholamine fluorescence, a method used to visualize these chemicals, in specific areas.
- Administering alpha-MPT to the rats, however, did not significantly modify their growth rate or the timing of puberty. Regular oestrous cycle occurred after puberty in animals treated with either 6-OHDA or alpha-MPT.
- Different techniques of administering 6-OHDA (with or without DMI or pargyline) showed varied results on the surge of LH and GnRH hormones induced by pregnant mare serum gonadotropin (PMSG), a hormone preparation from pregnant mares.
Research Implications
- These findings show a considerable difference in the long-term and short-term effects of 6-OHDA on the gonadotropin control system, which regulates hormone production.
- Neonatal treatment with 6-OHDA plus DMI notably delays the commencement of puberty and the rate of body growth, but does not affect cyclical gonadotropin release and has no unchanging effect on the hypothalamic catecholaminergic systems.
- The research suggests that catecholamines play a crucial role in puberty and reproductive hormone production in rats, which could have broader implications for understanding human puberty and fertility.
Cite This Article
APA
Sarkar DK, Smith GC, Fink G.
(1981).
Effect of manipulating central catecholamines on puberty and the surge of luteinizing hormone and gonadotropin releasing hormone induced by pregnant mare serum gonadotropin in female rats.
Brain Res, 213(2), 335-349.
https://doi.org/10.1016/0006-8993(81)90239-0 Publication
Researcher Affiliations
MeSH Terms
- Animals
- Body Weight / drug effects
- Brain / drug effects
- Brain / metabolism
- Catecholamines / metabolism
- Female
- Gonadotropin-Releasing Hormone / metabolism
- Gonadotropins, Equine / pharmacology
- Hydroxydopamines / pharmacology
- Luteinizing Hormone / metabolism
- Methyltyrosines / pharmacology
- Rats
- Sexual Maturation / drug effects
- Tyrosine 3-Monooxygenase / antagonists & inhibitors
- Vagina / drug effects
- Vagina / physiology
- alpha-Methyltyrosine
Citations
This article has been cited 13 times.- Street ME, Ponzi D, Renati R, Petraroli M, D'Alvano T, Lattanzi C, Ferrari V, Rollo D, Stagi S. Precocious puberty under stressful conditions: new understanding and insights from the lessons learnt from international adoptions and the COVID-19 pandemic.. Front Endocrinol (Lausanne) 2023;14:1149417.
- Dees WL, Hiney JK, Srivastava VK. How alcohol affects insulin-like growth factor-1's influences on the onset of puberty: A critical review.. Alcohol Clin Exp Res 2021 Nov;45(11):2196-2206.
- Dees WL, Hiney JK, Srivastava VK. IGF-1 Influences Gonadotropin-Releasing Hormone Regulation of Puberty.. Neuroendocrinology 2021;111(12):1151-1163.
- Hiney JK, Srivastava VK, Vaden Anderson DN, Hartzoge NL, Dees WL. Regulation of Kisspeptin Synthesis and Release in the Preoptic/Anterior Hypothalamic Region of Prepubertal Female Rats: Actions of IGF-1 and Alcohol.. Alcohol Clin Exp Res 2018 Jan;42(1):61-68.
- Hiney JK, Srivastava VK, Dees WL. Manganese protects against the effects of alcohol on hypothalamic puberty-related hormones.. Life Sci 2016 Mar 1;148:106-11.
- Hiney JK, Srivastava VK, Volz CE, Dees WL. Alcohol alters insulin-like growth factor-1-induced transforming growth factor β1 synthesis in the medial basal hypothalamus of the prepubertal female rat.. Alcohol Clin Exp Res 2014 Oct;38(10):2572-8.
- Srivastava VK, Hiney JK, Dees WL. Actions and interactions of alcohol and transforming growth factor β1 on prepubertal hypothalamic gonadotropin-releasing hormone.. Alcohol Clin Exp Res 2014 May;38(5):1321-9.
- Semaan SJ, Murray EK, Poling MC, Dhamija S, Forger NG, Kauffman AS. BAX-dependent and BAX-independent regulation of Kiss1 neuron development in mice.. Endocrinology 2010 Dec;151(12):5807-17.
- Srivastava VK, Hiney JK, Dees WL. Prepubertal ethanol exposure alters hypothalamic transforming growth factor-α and erbB1 receptor signaling in the female rat.. Alcohol 2011 Mar;45(2):173-81.
- Dees WL, Srivastava V, Hiney JK. Actions and interactions of alcohol and insulin-like growth factor-1 on female pubertal development.. Alcohol Clin Exp Res 2009 Nov;33(11):1847-56.
- Dluzen D, Attaran M, Liu B. The effect of estrogen administration in vivo upon catecholamine release in vitro from superfused hypothalamic tissue of ovariectomized pre-pubertal and adult mice.. J Endocrinol Invest 1994 Dec;17(11):855-60.
- Becú-Villalobos D, Libertun C. Development of gonadotropin-releasing hormone (GnRH) neuron regulation in the female rat.. Cell Mol Neurobiol 1995 Feb;15(1):165-76.
- Minami S, Frautschy SA, Plotsky PM, Sutton SW, Sarkar DK. Facilitatory role of neuropeptide Y on the onset of puberty: effect of immunoneutralization of neuropeptide Y on the release of luteinizing hormone and luteinizing-hormone-releasing hormone.. Neuroendocrinology 1990 Jul;52(1):112-5.
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