115. Central Neuronal Control of Bone Remodeling

  1. Clifford J. Rosen MD
  1. Shu Takeda and
  2. Paul Baldock

Published Online: 19 JUL 2013

DOI: 10.1002/9781118453926.ch115

Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, Eighth Edition

Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, Eighth Edition

How to Cite

Takeda, S. and Baldock, P. (2013) Central Neuronal Control of Bone Remodeling, in Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, Eighth Edition (ed C. J. Rosen), John Wiley & Sons, Inc., Ames, USA. doi: 10.1002/9781118453926.ch115

Publication History

  1. Published Online: 19 JUL 2013

ISBN Information

Print ISBN: 9781118453889

Online ISBN: 9781118453926

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Keywords:

  • bone remodeling;
  • central neuronal control;
  • leptin;
  • melanocortins;
  • neuromedin U (NMU);
  • neuropeptide Y system;
  • NPY receptors;
  • serotonin;
  • sympathetic nervous system

Summary

Clinical evidence that traumatic brain injury (TBI) accelerates the healing of fractures suggests that there is a link between the central nervous system and bone remodeling. The discovery that leptin regulates bone formation through the central nervous system initiated a new research field: neuronal control of bone remodeling. Since then, other neuropeptides and neurotransmitters, such as neuropeptide Y (NPY), cocaine- and amphetamine-regulated transcript (CART), neuromedin U, and, more recently, serotonin, have been demonstrated to possess bone-regulating activities. Melanocortins are a complex family comprising a number of endogenous agonists that are all derived from a single precursor, pro-opiomelanocortin (POMC), of which α-, β- and γ-MSH (melanocyte-stimulating hormone) and adrenocorticotropic hormone (ACTH) elicit their action by interacting with five melanocortin receptors (MCRs), identified as G-protein coupled receptors MCR1—5.