Gastric distention induced functional magnetic resonance signal changes in the rodent brain.

Neuroscience

Gastrointestinal Research Group, Department of Production Animal Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada.

Published: April 2011

Investigating the localization of gastric sensation within the brain is important for understanding the neural correlates of satiety. Previous rodent studies have identified the brain-stem and hypothalamus as key mediators of gastric distention-induced satiation. Although, recent blood oxygen level-dependent functional magnetic resonance imaging (BOLD fMRI) studies in humans have identified a role for higher cortico-limbic structures in mediating the satiation effects of gastric distention, the role of these regions in rodents remains to be characterized. We determined the effects of gastric distention on global spatio-temporal BOLD fMRI signal changes in the rodent brain. Brain images were acquired with a high resolution 9.4 T magnet during gastric distention with continuous monitoring of blood pressure in adult male Sprague Dawley rats (n=8-10). Distention of the stomach with an intragastric balloon, at rates which mimicked the rate of consumption and emptying of a mixed nutrient liquid meal, resulted in robust reduction in food intake and increase in blood pressure. Gastric distention increased BOLD fMRI activity within homeostatic regions such as the hypothalamus and nucleus tractus solitarius, as well as non homeostatic regions including the hippocampus, amygdala, thalamus, cerebellum and the cortex (cingulate, insular, motor and sensory cortices). Further, the increase in BOLD fMRI activity following distention was strongly correlated to an increase in blood pressure. These results indicate that gastric distention, mimicking the rate of intake and emptying of a liquid meal, increases BOLD fMRI activity in both homeostatic and non homeostatic brain circuits which regulate food intake, and that these BOLD fMRI signal changes may in part be attributable to transient increases in blood pressure.

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Source
http://dx.doi.org/10.1016/j.neuroscience.2011.01.051DOI Listing

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