Changes in Alpha-Melanocyte-Stimulating Hormone Content in Discrete Hypothalamic Areas of the Male Rat during a Twenty-Four-Hour Period

Scimonelli, Teresa Nieves; Celis, M.E.; Eberlé, Alex N.

doi:10.1159/000180792

Cited by 9 publications

(5 citation statements)

References 17 publications

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“…The existence of E-box-binding sites in the promoter region of the POMC gene (Fig. 4) lends further support to the hypothesis of transcriptional regulatory control similar to that found in the brain and points to avenues of future direction (O'Donohue et al 1979a,b, Monnet et al 1981, Scimonelli et al 1987.…”

Section: Neuropeptides Insupporting

confidence: 67%

Diurnal profiling of neuroendocrine genes in murine heart, and shift in proopiomelanocortin gene expression with pressure-overload cardiac hypertrophy

Chalmers¹,

Lin²,

Martino³

et al. 2008

Journal of Molecular Endocrinology

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Neuroendocrine peptides express biologic activity relevant to the cardiovascular system, including regulating heart rate and blood pressure, though little is known about the mechanisms involved. Here, we investigated neuroendocrine gene expression underlying diurnal physiology of the heart. We first used microarray and RT-PCR analysis and demonstrate the simultaneous expression of neuroendocrine genes in normal murine heart, including POMC, GnRH, neuropeptide Y, leptin receptor, GH-releasing hormone, cocaine-and amphetamine-regulated transcript, proglucagon, and galanin. We examined diurnal gene expression profiles, with cosinar bioinformatics to evaluate statistically significant rhythms. The POMC gene exhibits a day/night, circadian or diurnal, pattern of expression in heart, and we postulated that this may be important to cardiac growth and renewal. POMC diurnal gene rhythmicity is altered in pressure-overload cardiac hypertrophy, when compared with control heart, and levels increased at the dark-to-light transition times. These findings are also consistent with the proposal that neuropeptides mediate adverse remodeling processes, such as occur in pathologic hypertrophy. To investigate cellular responses, we screened three cell lines representing fibroblasts, cardiac myocytes, and vascular smooth muscle cells (NIH3T3, heart line 1, and mouse vascular smooth muscle cell line 1 (Movas-1) respectively). POMC mRNA expression is the most notable in Movas-1 cells and, furthermore, exhibits rhythmicity with culture synchronization. Taken together, these results highlight the diverse neuroendocrine mRNA expression profiles in cardiovasculature, and provide a novel model vascular culture system to research the role these neuropeptides play in organ health, integrity, and disease.

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Section: Neuropeptides Insupporting

confidence: 67%

Diurnal profiling of neuroendocrine genes in murine heart, and shift in proopiomelanocortin gene expression with pressure-overload cardiac hypertrophy

Chalmers¹,

Lin²,

Martino³

et al. 2008

Journal of Molecular Endocrinology

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“…Radioimmunoassay for a-MSH a-MSH was measured by radioimmunoassay as described previously (Scimonelli et al 1987). The sensitivity of the assay was about 2-5pg/tube.…”

Section: Blood Collectionmentioning

confidence: 99%

The effect of the blockade of α-melanocyte-stimulating hormone on LH release in the rat

Caballero

Celis²

1993

Journal of Endocrinology

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We have investigated the effect of blocking alpha-MSH on the release of LH in rats at pro-oestrus. Continuous infusion of Pro-Leu-Gly-NH2 (PLG; 0.2 microgram/h), from the afternoon of dioestrus-2 until the day of oestrus, inhibited LH at pro-oestrus and the next ovulation on the day of oestrus. Plasma alpha-MSH levels decreased significantly in rats treated with PLG. This inhibitory effect on LH release was not observed in rats treated with a continuous infusion of a diluted antiserum against alpha-MSH (0.5 microliter/h, diluted 1/10) from the afternoon of dioestrus-2 until the day of oestrus. On the contrary, the administration of undiluted antiserum against alpha-MSH (0.5 microliter/h) blocked LH release and ovulation. The release of alpha-MSH into the blood was also significantly blocked by this treatment. When serum levels of progesterone were measured at 12.00 and 14.00 h in rats in which alpha-MSH release was blocked by PLG or concentrated antiserum, a significant decrease was observed when compared with the levels of progesterone in control rats. These results show that the blockade of alpha-MSH inhibits LH release and the next ovulation in rats treated with PLG or with concentrated antiserum against alpha-MSH, through a blockade of progesterone of adrenal origin.

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“…The circadian variations in a-MSH in the pituitary and in different brain areas are not synchronous. Even in different hypothalamic nuclei there are mutual differ ences in the diurnal variations in a-MSH levels [19][20][21], A similar conclusion has been reached by de Rotte et al [22], This demonstates that the a-MSH in the plasma, which is of pituitary origin, and that in the cerebrospinal fluid, which might originate from the central nervous sys tem, could be regulated by different mechanisms. It is possible that dopamine acts postsynaptically on a-MSHcontaining cells in the pituitary and presynaptically in the hippocampus.…”

Section: Discussionmentioning

confidence: 62%

Effects of Cocaine and Pimozide on Plasma and Brain Alpha-Melanocyte-Stimulating Hormone Levels in Rats

Sarnyai¹,

Vecsernyés

Julesz

et al. 1992

Neuroendocrinology

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The effects of cocaine on rat plasma and brain α-melanocyte-stimulating hormone (α-MSH) levels have been studied by means of a specific radioimmunoassay. The selected brain areas were the hypothalamus, septum-nucleus ac-cumbens and hippocampus. Cocaine given subcutaneously decreased the α-MSH levels in the peripheral blood. Pimozide, a dopaminergic antagonist, had an opposite effect: it increased the α-MSH levels in the peripheral blood. Combined treatment with cocaine + pimozide resulted in a decrease in the pimozide-induced increase in α-MSH levels in the blood. Cocaine and pimozide or the combination of cocaine + pimozide were ineffective on the α-MSH levels in the hypothalamus and septum-accumbens brain regions. In the hippocampus, cocaine in the dose applied induced a slight but not significant decrease in the α-MSH level. Pimozide caused a significant decrease in the hippocampal α-MSH level which disappeared at 60 min. Cocaine prevented the pimozide-induced depletion of α-MSH. The data indicate that cocaine may act as a dopaminergic agonist in the mechanism of control of α-MSH secretion from the intermediate lobe of the pituitary. The α-MSH levels in the brain are controlled by different mechanisms. In some brain areas, the dopaminergic system has no action; in others the mechanisms might be similar to but slightly different from that in the pituitary.

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Changes in Alpha-Melanocyte-Stimulating Hormone Content in Discrete Hypothalamic Areas of the Male Rat during a Twenty-Four-Hour Period

Cited by 9 publications

References 17 publications

Diurnal profiling of neuroendocrine genes in murine heart, and shift in proopiomelanocortin gene expression with pressure-overload cardiac hypertrophy

Diurnal profiling of neuroendocrine genes in murine heart, and shift in proopiomelanocortin gene expression with pressure-overload cardiac hypertrophy

The effect of the blockade of α-melanocyte-stimulating hormone on LH release in the rat

Effects of Cocaine and Pimozide on Plasma and Brain Alpha-Melanocyte-Stimulating Hormone Levels in Rats

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