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Previous Article | Next Article
The Journal of Neuroscience, August 15, 1999, 19(16):7130-7139
Changes in Neuropeptide Y Receptors and Pro-Opiomelanocortin in the Anorexia (anx/anx) Mouse Hypothalamus
Christian Broberger1, Jeanette Johansen2, Hjalmar Brismar3, Carolina Johansson2, Martin Schalling2, and Tomas Hökfelt1 Departments of 1 Neuroscience, 2 Molecular Medicine, and 3 Woman and Child Health, Karolinska Institutet, 171 77 Stockholm, Sweden
The pro-opiomelanocortinergic (POMCergic) system originating in the hypothalamic arcuate nucleus extends projections widely over the brain and has been shown to be intricately linked and parallel to the arcuate neuropeptide Y (NPY) system. Both NPY and POMC-derived peptides (melanocortins) have been strongly implicated in the control of feeding behavior, with the former exerting orexigenic effects and the latter having anorexigenic properties. Mice homozygous for the lethal anorexia (anx) mutation are hypophagic, emaciated, and exhibit anomalous processing of NPY exclusively in the arcuate nucleus, providing an interesting model to study NPY-POMC interactions. In the present study, several morphological markers were used to investigate the histochemistry and morphology of the POMC system in anx/anx mice. In situ hybridization demonstrated decreased numbers of POMC mRNA-expressing neurons in the anx/anx arcuate nucleus. In parallel, mRNA levels for both the NPY Y1 and Y5 receptors, which are expressed in POMC neurons, were decreased. Also, expression of the NPY Y2 autoreceptor was attenuated. Immunohistochemistry using antibodies against adrenocorticotropic hormone to demonstrate POMC cell bodies, against
-melanocyte-stimulating hormone to demonstrate axonal projections and against the NPY Y1 receptor to demonstrate dendritic arborizations, showed strikingly decreased immunoreactivities for all these markers. The present data suggest that degeneration of the arcuate POMC system is a feature characteristic of the anx/anx mouse. The possible relationship to the NPYergic phenotype of this animal is discussed.
Key words: adrenocorticotropic hormone;
Copyright © 1999 Society for Neuroscience 0270-6474/99/19167130-10$05.00/0
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