Detection of neuronal activity and metabolism in a model of dehydration-induced anorexia in rats at 14.1 T using manganese-enhanced MRI and 1H MRS
Article first published online: 4 MAY 2011
Copyright © 2011 John Wiley & Sons, Ltd.
NMR in Biomedicine
Volume 24, Issue 10, pages 1326–1336, December 2011
How to Cite
Just, N. and Gruetter, R. (2011), Detection of neuronal activity and metabolism in a model of dehydration-induced anorexia in rats at 14.1 T using manganese-enhanced MRI and 1H MRS. NMR Biomed., 24: 1326–1336. doi: 10.1002/nbm.1694
- Issue published online: 3 JAN 2012
- Article first published online: 4 MAY 2011
- Manuscript Accepted: 19 JAN 2011
- Manuscript Revised: 18 NOV 2010
- Manuscript Received: 14 JUN 2010
- Dehydration Induced Anorexia;
In this study, hypothalamic activation was performed by dehydration-induced anorexia (DIA) and overnight food suppression (OFS) in female rats. The assessment of the hypothalamic response to these challenges by manganese-enhanced MRI showed increased neuronal activity in the paraventricular nuclei (PVN) and lateral hypothalamus (LH), both known to be areas involved in the regulation of food intake. The effects of DIA and OFS were compared by generating T-score maps. Increased neuronal activation was detected in the PVN and LH of DIA rats relative to OFS rats. In addition, the neurochemical profile of the PVN and LH were measured by 1H MRS at 14.1 T. Significant increases in metabolite levels were measured in DIA and OFS relative to control rats. Statistically significant increases in γ-aminobutyric acid were found in DIA (p = 0.0007) and OFS (p < 0.001) relative to control rats. Lactate increased significantly in DIA (p = 0.03), but not in OFS, rats. This work shows that manganese-enhanced MRI coupled to 1H MRS at high field is a promising noninvasive method for the investigation of the neural pathways and mechanisms involved in the control of food intake, in the autonomic and endocrine control of energy metabolism and in the regulation of body weight. Copyright © 2011 John Wiley & Sons, Ltd.