Gastrointestinal Research Group, Department of Production Animal Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada.
Neuroscience. 2011 Apr 14;179:151-8. doi: 10.1016/j.neuroscience.2011.01.051. Epub 2011 Feb 1.
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.
研究胃感觉在大脑中的定位对于理解饱腹感的神经相关性非常重要。先前的啮齿动物研究已经确定脑干和下丘脑是胃扩张引起饱腹感的关键中介。尽管最近人类基于血氧水平依赖的功能磁共振成像（BOLD fMRI）研究已经确定了皮质-边缘结构在介导胃扩张引起的饱腹感效应中的作用，但这些区域在啮齿动物中的作用仍有待确定。我们确定了胃扩张对啮齿动物大脑全局时空 BOLD fMRI 信号变化的影响。在成年雄性 Sprague Dawley 大鼠（n=8-10）中，使用高分辨率 9.4 T 磁铁进行胃扩张期间获取脑图像，并连续监测血压。通过向胃内充气的方式进行胃扩张，充气速度模拟混合营养液体餐的摄入和排空速度，导致食物摄入量明显减少和血压升高。胃扩张增加了下丘脑和孤束核等稳态区域以及非稳态区域（包括海马体、杏仁核、丘脑、小脑和大脑皮层（扣带回、岛叶、运动和感觉皮层）的 BOLD fMRI 活性。此外，扩张后 BOLD fMRI 活性的增加与血压的增加呈强烈相关。这些结果表明，模仿液体餐摄入和排空速度的胃扩张增加了调节食物摄入的稳态和非稳态脑回路中的 BOLD fMRI 活性，并且这些 BOLD fMRI 信号变化部分可能归因于血压的短暂升高。
