Abstract
We tested whether MC4R null mice display altered gustatory function relative to wild-type controls that may contribute to the characteristic hyperphagia and obesity associated with this gene deletion. Mice were tested for their licking responses to prototypical taste solutions (sucrose, NaCl, quinine, citric acid) in series of daily 30-min sessions in which a range of concentrations of each tastant was available in randomized blocks of 5-s trials. Notwithstanding some minor deviations, the concentration-response functions of the MC4R null and wild-type mice were basically the same for all of the prototypical compounds tested here. Thus, taste-based appetitive and avoidance behavior is expressed in the absence of the MC4 receptor, demonstrating that this critical component in the melanocortin system is not required for normal affective gustatory function to be maintained.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1712-1719 |
| Number of pages | 8 |
| Journal | Peptides |
| Volume | 26 |
| Issue number | 10 |
| DOIs | |
| State | Published - Oct 2005 |
Bibliographical note
Funding Information:We would like to thank Ginger Blonde, Mary Clinton, John Leftwich, and Angela Newth for technical assistance. The MC4R KO mice were graciously provided by Dr. Dennis Huszar at Millennium Pharmaceuticals. This research was supported by a grant from the National Institute on Deafness and Other Communication Disorders (R01-DC04574) to A.C.S. and the National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK57080) to C.H.-L.
Keywords
- Citric acid
- Gustatory
- Hedonics
- Hyperphagia
- Knockout mice
- NaCl
- Neuropeptides
- Obesity
- Quinine
- Sucrose
