An Improved Radioimmunoassay for &lt;i&gt;α&lt;/i&gt;-Melanocyte-Stimulating Hormone (&lt;i&gt;α&lt;/i&gt;-MSH) in the Rat: Serum and Pituitary &lt;i&gt;α&lt;/i&gt;-MSH Levels after Drugs Which Modify Catecholaminergic Neurotransmission

Penny, R.J.; Thody, A. J.

doi:10.1159/000122741

Cited by 83 publications

(32 citation statements)

References 10 publications

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“…Moreover, the pituitary content of both peptides seems responsive to the mode of delivery suggesting that a melanotropic stress-related circuitry is already established from midgestation (15). Domperidone, an antagonist of dopamine receptors, was able to stimulate both a-MSH and ACTH 1-13 plasma levels, in the present study, in agreement with the well-known inhibitory role exerted by dopamine on a-MSH release in different species (11,17,18). However, domperidone-induced melanotropic hormone release is evident in prepubertal children although absent in pubertal boys and girls, suggesting an enhanced dopaminergic tone and/or an increased sensitivity to dopamine antagonist, in prepubertal life.…”

Section: Discussionsupporting

confidence: 89%

Changes in Dopaminergic Control of Circulating Melanocyte-Stimulating Hormone-Related Peptides at Puberty

et al. 1995

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Desacetyl a-melanocyte-stimulating hormone (MSH) (ACTH 1-13) is the main form of immunoreactive a-MSH circulating in human plasma. This study evaluates the possibility that a dopaminergic inhibitory mechanism could be operative during human development. Thus, a-MSH and ACTH 1-13 plasma levels were measured after dopaminergic blockade (domperidone (0.3 m a g body weight, maximum 10 mg, p.0.) in 13 prepubertal (aged 4.5-12.3 y) and 12 pubertal (aged 10.2-16.9 y) children. Both peptides were measured by RIA after plasma extraction on Sep-pak C-18 cartridges and reverse phase HPLC. The chromatographic profile of a-MSH immunoreactivity falls into two main peaks, corresponding to the retention time of a-MSH and ACTH 1-13. Moreover, in prepubertal children domperidone induced a significant increase of a-MSH from 1.7 (median) to 5.0 pmol/L, whereas no changes in a-MSH plasma levels were found in pubertal subjects (from 5.0 to 4.1 pmol/L). Similarly, ACTH 1-13 plasma levels significantly increased from 3.0 to 19.8 pmol/L in prepubertal children remaining stable in pubertal ones (from 7.8 to 4.6 pmol/L). Moreover, a significant negative correlation was found between basal DHEA-S levels and the plasma a-MSH increase after domperidone. These data demonstrate that: 1 ) ACTH 1-13 is the main form of immunoreactive a-MSH in prepubertal life and 2) the dopaminergic inhibition of both ACTH 1-13 and a-MSH plasma levels is apparent only in prepubertal subjects. (Pediatr Res 38: 91-94, 1995) Abbreviations a-MSH, a-melanocyte-stimulating hormone ACTH 1-13, desacetyl a-melanocyte-stimulating hormone POMC, proopiomelanocortin DHEA-S, dehydroepiandrosterone sulfate a-MSH is a peptide deriving from a two steps cleavage of POMC for the formation of which the activity of a-Nacetyltransferase is required (1). In lower mammals, these enzymatic events are absent from the anterior pituitary, whereas they are typical of the neurointermediate lobe, which is well developed in these species (2). In humans, the neurointermediate lobe is virtually absent in adults (3), whereas it has been detected in the fetal pituitary (4) and in a subgroup of patients with Cushing's disease (5).In contrast to the studies of late 1970s, detectable levels of a-MSH plasma have been found in healthy adult volunteers (6, 7), and they have been found higher than normal in patients affected by Cushing disease (8). The results of the abovementioned studies were obtained coupling the classical a-MSH RIA to purification procedures, such as extraction and HPLC, and revealed that the des-acetylated form of a-MSH (i.e. ACTH 1-13 amide) is the main form of plasma immunoreactive a-MSH. This finding also suggests a possible functional activity of neurointermediate lobe in some physiopathologic conditions.We previously demonstrated that, in contrast to ACTH levels, plasma P-endorphin concentrations increased progressively throughout prepuberty, reaching adult levels at the beginning of pubertal development (9). These data were in keeping with the suggested role of POMC-related...

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Section: Discussionsupporting

confidence: 89%

Changes in Dopaminergic Control of Circulating Melanocyte-Stimulating Hormone-Related Peptides at Puberty

et al. 1995

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“…Severing neurons in the retrochiasmatic region of the hypothalamus blocked the stress-induced decrease in DOPAC/DA in the intermediate lobe and attenuated the stress-induced increase in plasma concentrations of a-MSH. Taken together, these results indicate that a decrease in tuberohypophysial dopaminergic neuronal inhibitory tone and an increase in [4,5,7,8]. Under nonstressed basal conditions, a-MSH secretion is tonically inhibited by dopamine (DA) released from tubero hypophysial neurons which project from the arcuate nucleus [9] or the periventricular nucleus of the rostral hypothalamus to the intermediate lobe [10].…”

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confidence: 90%

Dopaminergic and Beta-Adrenergic Receptor Control of Alpha-Melanocyte-Stimulating Hormone Secretion during Stress

Lindley

Lookingland²,

Moore³

1990

Neuroendocrinology

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The relative roles of dopaminergic and β-adrenergic receptors in mediating the stress-induced increase in the secretion of α-melanocyte-stimulating hormone (α-MSH) from the intermediate lobe of the pituitary were determined in the male rat. Thirty minutes of physical immobilization (restraint stress) increased the circulating concentrations of α-MSH and decreased the 3,4-dihydroxyphenylacetic acid/dopamine (DOPAC/DA) ratio in the intermediate lobe of the pituitary, reflecting a decrease in the tuberohypophysial dopaminergic neuronal activity. Pretreatment with the β-adrenergic antagonist propranolol reduced the stress-induced increase in the circulating levels of α-MSH, but had no effect on the basal plasma concentrations of this hormone or the stress-induced decrease in DOPAC/DA in the intermediate lobe. If the dopaminergic tone during stress was maintained by administration of the DA agonist apomorphine, the stress-induced increase in α-MSH secretion was prevented. In nonstressed animals the administration of the β2-adrenergic agonist metaproterenol increased the plasma levels of α-MSH, and the effect of this drug was augmented if the inhibitory dopaminergic tone on α-MSH secretion was blocked by the administration of the DA antagonist haloperidol. Severing neurons in the retrochiasmatic region of the hypothalamus blocked the stress-induced decrease in DOPAC/DA in the intermediate lobe and attenuated the stress-induced increase in plasma concentrations of α-MSH. Taken together, these results indicate that a decrease in tuberohypophysial dopaminergic neuronal inhibitory tone and an increase in β-adrenergic stimulation are both necessary for the full expression of the stress-induced increase in secretion of α-MSH from melanotrophs in the intermediate lobe of the rat pituitary.

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“…AgRP and MSH are also present in the systemic circulation (Penny & Thody 1978, Li et al 2000. The function of circulating AgRP and MSH along with the peripheral roles of melanocortins and their receptors remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Peripherally administered [Nle4,d-Phe7]-α-melanocyte stimulating hormone increases resting metabolic rate, while peripheral agouti-related protein has no effect, in wild type C57BL/6 and ob/ob mice

Hoggard¹,

Rayner²,

Johnston³

et al. 2004

Journal of Molecular Endocrinology

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7]--melanocyte stimulating hormone increases resting metabolic rate, while peripheral agouti-related protein has no effect, in wild type C57BL/6 and ob/ob mice AbstractThe melanocortin system coordinates the maintenance of energy balance via the regulation of both food intake and energy expenditure. Leptin, a key adipogenic hormone involved in the regulation of energy balance is thought to act by stimulating production, in the hypothalamic arcuate nucleus, of -melanocyte stimulating hormone ( MSH), a potent agonist of MC3/4 melanocortin receptors located in the paraventricular nucleus of the hypothalamus. Additionally leptin inhibits release of agouti-related protein (AgRP), an MC4R antagonist. During periods of caloric restriction, weight loss is not sustained because compensatory mechanisms, such as reduced resting metabolic rate (RMR) are brought into play. Understanding how these compensatory systems operate may provide valuable targets for pharmaceutical therapies to support traditional dieting approaches. As circulating leptin is reduced during caloric restriction, it may mediate some of the observed compensatory responses. In addition to decreases in circulating leptin levels, circulating AgRP is increased during fasting in rodents while MSH is decreased. As central administration of AgRP depresses metabolism, we hypothesised that the peripheral rise in AgRP might be involved in signalling the depression of RMR during food restriction. We hypothesised that changes in plasma AgRP and MSH may coordinate the regulation of changes in energy expenditure acting through central MC4 melanocortin receptors via the sympathetic nervous system. We show here that acute peripherally administered AgRP at supra-physiological concentrations in both lean (C57BL/6) and obese leptin-deficient (ob/ob) mice does not depress RMR, possibly because it crosses the blood-brain barrier very slowly compared with other metabolites. However, in vitro AgRP can decrease leptin secretion, by approximately 40%, from adipocytes into culture medium and may via this axis have an effect on energy metabolism during prolonged caloric restriction. In contrast, peripheral [Nle 4 ,D-Phe 7 ]-MSH produced a large and sustained increase in resting energy expenditure (0·15 ml O 2 /min; P,0·05) with a similar response in leptin-deficient ob/ob mice (0·27 ml O 2 /min) indicating that this effect is independent of the status of leptin production in the periphery. In both cases respiratory exchange ratio and the levels of energy expended on spontaneous physical activity were unaffected by the administration of peripheral [Nle 4 ,D-Phe 7 ]-MSH. In conclusion, MSH analogues that cross the blood-brain barrier may significantly augment dietary restriction strategies by sustaining elevated RMR.

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An Improved Radioimmunoassay for <i>α</i>-Melanocyte-Stimulating Hormone (<i>α</i>-MSH) in the Rat: Serum and Pituitary <i>α</i>-MSH Levels after Drugs Which Modify Catecholaminergic Neurotransmission

Cited by 83 publications

References 10 publications

Changes in Dopaminergic Control of Circulating Melanocyte-Stimulating Hormone-Related Peptides at Puberty

Changes in Dopaminergic Control of Circulating Melanocyte-Stimulating Hormone-Related Peptides at Puberty

Dopaminergic and Beta-Adrenergic Receptor Control of Alpha-Melanocyte-Stimulating Hormone Secretion during Stress

Peripherally administered [Nle4,d-Phe7]-α-melanocyte stimulating hormone increases resting metabolic rate, while peripheral agouti-related protein has no effect, in wild type C57BL/6 and ob/ob mice

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