Anorexigenic melanocortin signaling in the hypothalamus is augmented in association with failure-to-thrive in a transgenic mouse model for Prader-Willi syndrome.
In: Brain research, Jg. 957 (2002-12-06), Heft 1, S. 42-5
academicJournal
Zugriff:
As in Prader-Willi syndrome (PWS) infants, mouse models of PWS display failure-to-thrive during the neonatal period. In rodents, the hypothalamic neuropeptide, Neuropeptide Y (NPY) and Agouti-related peptide (AgrP) stimulate while alpha-melanocyte stimulating hormone (alpha-MSH) inhibits appetite. We hypothesized that altered expression of these neuropeptides in the hypothalamus may underlie the failure-to-thrive in PWS neonatal mice. To test this hypothesis we evaluated mRNA expression of Npy, Agrp, and Pomc by in situ hybridization in the hypothalamic arcuate nucleus (ARC) of 3-day-old female and male PWS neonates. The results showed that Agrp mRNA expression was decreased relative to wild-type (WT) controls in neonates of both sexes, while mRNA expression of Pomc was upregulated in PWS neonates. Since AgrP and the Pomc-derived peptide, alpha-MSH, are functional antagonists at melanocortin 4 receptors in the hypothalamic regulation of appetitive behavior, these results show that robust anorexigenic melanocortin signaling, may contribute to the failure-to-thrive in PWS neonatal mice.
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Anorexigenic melanocortin signaling in the hypothalamus is augmented in association with failure-to-thrive in a transgenic mouse model for Prader-Willi syndrome.
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Autor/in / Beteiligte Person: | Ge, Y ; Ohta, T ; Driscoll, DJ ; Nicholls, RD ; Kalra, SP |
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Zeitschrift: | Brain research, Jg. 957 (2002-12-06), Heft 1, S. 42-5 |
Veröffentlichung: | Amsterdam Elsevier/North-Holland Biomedical Press., 2002 |
Medientyp: | academicJournal |
ISSN: | 0006-8993 (print) |
DOI: | 10.1016/s0006-8993(02)03583-7 |
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