Voluntary exercise modulation of olfactory function

摘要 我们实验室以前的研究已经发现，摄入高脂肪饮食会导致 小鼠的嗅觉感觉神经元。自愿运动已被证明可以保护几个大脑区域的神经元， 不同类型的伤害。本项目的主要目标是确定参与自愿运动是否 能够保护嗅觉系统的神经元免受脂肪饮食的有害影响。超出 保护，我还打算确定是否自愿运动的良好神经调节作用延伸到 嗅觉系统将嗅觉障碍与神经退行性疾病相关联的证据，如 阿尔茨海默氏症，继续增长，因此，重要的是要研究饮食和运动对老年痴呆症的影响。 这个经常被忽视的感觉系统。这些研究将通过改变饮食组成来完成， 肥胖症，应用成对喂养来控制体重增加，提供一个家庭笼运行轮， 组织学分析以确定解剖学变化，以及电生理学分析以评估细胞内 生物物理特性这些实验的基础是这样一种假设，即高脂肪饮食会引起炎症。 环境对小鼠嗅觉系统的损害和自主运动是嗅觉神经调节剂 如果允许老鼠参加这样的运动，同时它们以脂肪食物为生， 饮食.研究这一假设的具体目的是：1）确定摄入不含脂肪的饮食是否 过度消费，因此没有伴随的体重增加，足以减少嗅觉感觉神经元 丰度及其相关的轴突投射。2)为了确定自愿锻炼是否能够预防和/或 消除了由食用脂肪酸引起的嗅上皮和嗅球的结构损失， 饮食. 3)- 为了确定自愿运动是否改善了用脂肪酸刺激的小鼠中胰岛素调节的丧失， 饮食.嗅球初级神经元的电生理特性将被确定和比较。

ABSTRACT Previous efforts in our lab have uncovered that consumption of a fatty diet leads to a reduction in the number of olfactory sensory neurons in mice. Voluntary exercise has been shown to protect neurons in several brain areas from different types of injuries. The primary objective of this project is to determine if participation in voluntary exercise is capable of protecting the neurons of the olfactory system from the detrimental effects of a fatty diet. Beyond protection, I also intend to determine if the well-established neuromodulatory effects of voluntary exercise extend to the olfactory system. The evidence that associates olfactory disorders with neurodegenerative disorders, such as Alzheimer’s, continues to grow and for this reason it is important to investigate the effects of both diet and exercise on this oft-ignored sensory system. These studies will be accomplished through modification of diet composition to induce obesity, application of pair-feeding to manipulate body weight gain, provision of a home cage running wheel, histological analyses to determine anatomical changes, and electrophysiological analyses to assess changes in cellular biophysical properties. The basis of these experiments is the hypothesis that a fatty diet creates an inflammatory environment that damages the olfactory system of mice and voluntary exercise is a neuromodulator of the olfactory system that will prevent this damage if the mice are allowed to participate in such exercise while they subsist on a fatty diet. The specific aims designed to investigate this hypothesis are 1) To determine if ingestion of a fatty diet without overconsumption, and therefore without the concomitant weight gain, is sufficient to decrease olfactory sensory neuron abundance and their correlate axonal projections. 2) To determine if voluntary exercise is capable of preventing and/or abrogating the structural loss in the olfactory epithelium and olfactory bulb that is caused by consumption of a fatty diet. 3) – To determine if voluntary exercise ameliorates the loss of insulin modulation in mice challenged with a fatty diet. Electrophysiological properties of the olfactory bulb primary neurons will be determined and compared.