| First Author | Vollmer RR | Year | 2006 |
| Journal | Exp Neurol | Volume | 202 |
| Issue | 2 | Pages | 441-8 |
| PubMed ID | 16930592 | Mgi Jnum | J:144672 |
| Mgi Id | MGI:3831491 | Doi | 10.1016/j.expneurol.2006.07.006 |
| Citation | Vollmer RR, et al. (2006) Sodium ingestion in oxytocin knockout mice. Exp Neurol 202(2):441-8 |
| abstractText | Under certain circumstances, central oxytocin (OT) pathways inhibit dietary intake of NaCl in rats and mice. C57BL/6 OT knockout (OT KO) mice were reported to consume greater amounts of saline solution than wild type (WT) cohorts when both were water deprived overnight. In this study, we determined that OT KO and WT mice of C57BL/6 strain demonstrate an equivalent taste aversion for continuously available 0.2 M, 0.3 M or 0.5 M NaCl. The aversion was proportional to the concentration of NaCl, similar to what has been reported in rats. Furthermore, OT KO and WT animals ingested the same daily amounts of a low, 0.01%, regular, 1.0%, and a high, 8.0%, NaCl diet that was provided ad libitum as a single choice. While consuming these diets, mice were given the choice to drink water or saline (0.5 M NaCl). As the amount of NaCl in the diet increased, mice of both genotypes significantly decreased the consumption of saline solution to an equal degree. Additionally, in an experimental model of sustained dehydration previously developed in rats, 0.5 M NaCl was the only available drinking fluid. Like rats subjected to this paradigm, OT KO and WT mice decreased food intake, decreased body weight and increased fluid ingestion with no genotypic differences. These findings suggest that oxytocinergic neuronal pathways cannot be the only regulator of ad libitum intake of NaCl in drinking solutions or diet. It appears that OT pathways may be more critical in controlling NaCl intake over brief intervals when an animal is quickly compensating for a dehydrating stimulus. |
