Journal article

Involvement of central relaxin-3 signalling in sodium (salt) appetite

Craig M Smith, Lesley L Walker, Berenice E Chua, Michael J McKinley, Andrew L Gundlach, Derek A Denton, Andrew J Lawrence

EXPERIMENTAL PHYSIOLOGY | WILEY | Published : 2015

Abstract

NEW FINDINGS: What is the central question of this study? Sodium appetite is controlled by conserved neuronal transmitter-receptor systems. Here, we tested the contribution made by relaxin family peptide 3 receptor (RXFP3), the cognate G-protein-coupled receptor for the neuropeptide relaxin-3. What is the main finding and its importance? Intracerebroventricular infusion of an RXFP3 antagonist reduced in a dose-dependent manner the volume of 0.3 m NaCl consumed by sodium-depleted C57Bl/6J (wild-type) mice. This effect was absent in sodium-depleted Rxfp3 knockout mice, and RXFP3 antagonist infusion did not alter water consumption in wild-type mice subjected to multiple thirst tests, indicating..

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Grants

Awarded by National Health and Medical Research Council of Australia


Awarded by NHMRC (Australia)


Funding Acknowledgements

This research was supported by National Health and Medical Research Council of Australia project grants 1079891 (A.J.L.), 1024885 (A.L.G.) and 1066939 (A.L.G.); NHMRC (Australia) Research Fellowships (1005985 and 1020737) to A.L.G. and A.J.L.; plus grants from the Pratt and Besen Family Foundations (A.L.G. and A.J.L.), a Brain & Behavior Research Foundation (USA) NARSAD Independent Investigator Award (A.L.G.) and the Victorian Government Operational Infrastructure Support Programme. This research was generously assisted by grants from The Mathers Charitable Foundation, The Search Foundation, Ms Diana Gibson, Mr S. Baillieu Myer, Dr Mark Nelson, Mr Robert Albert, Mr Andrew Abercrombie and Mrs Nielma Gantner (D.A.D.).