Authors: Skerry, T.M.; Taylor, A.F.

Source: Current Drug Metabolism, Volume 7, Number 8, 1 May 2001 , pp. 737-750(14)

Publisher: Bentham Science Publishers

Abstract:

The identification of novel signalling pathways in a tissue provides new avenues for pharmacological manipulation of tissue function. Where the pathway concerned is one that has been the subject of extensive research in another body system, progress towards new therapies can be rapid. The discovery that glutamate has functions in bone that share striking similarities with its role in synaptic neurotransmission opens the way to manipulate skeletal pathophysiology using modulators of glutamate release, uptake or receptor function. The purpose of this review is to describe the way that a role for glutamate as a signalling molecule in bone was discovered, to summarise the evidence for this role. In addition, it will identify points that are unresolved, to highlight areas where new research could provide significant advances. Furthermore, it will indicate how studies already performed but analysed without consideration of the non-neuronal functions of modulators of glutamate signalling, could contain information of significant value for the advance of therapeutic approaches to bone diseases.

Keywords: Glutamate Signalling; Bone; NEURONAL GLUTAMATE SIGNALLING; OSTEOBLASTSOSTEOBLASTS

Document Type: Review article

DOI: http://dx.doi.org/10.2174/1381612013397771

Publication date: 2001-05-01

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• Current Pharmaceutical Design publishes timely in-depth reviews covering all aspects of current research in rational drug design. Each issue is devoted to a single major therapeutic area. A Guest Editor who is an acknowledged authority in a therapeutic field has solicits for each issue comprehensive and timely reviews from leading researchers in the pharmaceutical industry and academia.
  
  Each thematic issue of Current Pharmaceutical Design covers all subject areas of major importance to modern drug design, including: medicinal chemistry, pharmacology, drug targets and disease mechanism.

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