Actions of neuropeptide Y and growth hormone secretagogues in the arcuate nucleus and ventromedial hypothalamic nucleus

Authors

  • Ekkasit Kumarnsit,

    1. School of Biomedical and Clinical Laboratory Sciences, College of Medical and Veterinary Sciences, The University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK
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  • Louise E. Johnstone,

    1. School of Biomedical and Clinical Laboratory Sciences, College of Medical and Veterinary Sciences, The University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK
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  • Gareth Leng

    1. School of Biomedical and Clinical Laboratory Sciences, College of Medical and Veterinary Sciences, The University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK
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: Professor Gareth Leng, as above.
E-mail: Gareth.Leng@ed.ac.uk

Abstract

Systemic or central administration of growth-hormone secretagogues (GHS) induces dense Fos expression in the arcuate nucleus but little or no Fos expression in the ventromedial hypothalamic nucleus, although both sites show intense expression of mRNA for the GHS receptor. Here, we recorded the electrical activity of single neurons from the arcuate nucleus and from the ventromedial hypothalamic nucleus in a rat hypothalamic slice preparation, and compared responses of these two populations to GHS. At both sites, the predominant neuronal response to GHS was a long-lasting excitation, indicating that GHS receptors at both sites are functional and similarly coupled to electrical excitation. We also tested neurons at both sites for their responses to neuropeptide Y and to somatostatin; at both sites the predominant response to each of these peptides was inhibitory. The arcuate cells that are activated by GHS include neuropeptide Y cells and growth hormone-releasing hormone cells. It seems possible that neuropeptide Y released in the ventromedial hypothalamus from the terminals of arcuate neurons counteracts the activation of ventromedial hypothalamic neurons by GHS in vivo, or that somatostatin released following liberation of growth hormone may do so.

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