Gustatory Processing of Free Fatty Acids

描述(申请人提供)：脂肪对生命至关重要，因为它促进器官的生长和发育，包括大脑。然而，过度摄入脂肪会导致肥胖。在这一点上，大多数动物(包括人类)更喜欢脂肪含量高的可口食物，这不是巧合。因此，脂肪的味道可能会增加对食物的好感。令人惊讶的是，很少有研究调查脂肪的味道。此外，大多数关于脂肪味道的研究都集中在对游离脂肪酸(FFAs)的行为反应上，而不是FFAs的神经编码。味觉鼓索神经(CT)参与了FFA检测，因为CT(CTX)的双侧横断显著削弱了对亚油酸(LA)的辨别，亚油酸是一种多不饱和脂肪酸，也是某些饮食脂肪的主要成分(Stratford等人，2006年)。然而，CT对LA的舌面应用无反应。因此，存在一个悖论，而CT在LA味觉辨别中的确切作用仍不清楚。这是特别相关的，因为对脂肪酸感知机制的理解可以为肥胖的发展提供洞察力。以下实验旨在利用平行的行为学和电泳学方法来确定CT在LA味觉反应中的作用。因为环磷酰胺扰乱了唾液分泌的神经控制，特定目标1将决定唾液腺和唾液钠浓度对脂肪味道的特定贡献。此外，由于脂肪传统上被认为是其他口味的增强剂，因此特定目标1也将检验添加LA将调节CT对其他口味刺激的电生理活动的假设。事实上，LA可能需要唾液(稀释的盐水)的背景来激活味觉细胞(即，味觉细胞无法对LA做出反应，除非环境中有一些低水平的钠)。这将在一定程度上解释我的行为数据(其中有唾液)和CT电生理数据(在水冲洗过程中唾液钠被冲洗掉)之间的差异。当添加LA时，CT对味觉刺激的反应发生变化，这表明LA调节了CT对其他味觉刺激的反应。最后，CTX没有取消LA的检测，这表明其他味觉神经也可能参与其中。具体目标2将使用味觉神经横断的条件味觉厌恶方案来确定外周味觉神经在LA味道中的作用。味觉神经切断后，LA味觉辨别能力受损，提示味觉神经参与了LA味觉检测。因此，这些数据提供了对脂肪味道在肥胖发展中的作用的洞察。

DESCRIPTION (provided by applicant): Fat is crucial for life as it promotes the growth and development of organs, including the brain. However, over consumption of fats can result in the development of obesity. In this regard, most animals (including humans) prefer savory foods that, not coincidental; have a high fat content. Thus, the taste of fat may enhance the favor of foods. Surprisingly, little research has investigated the taste of fat. Moreover, most research on fat taste has focused on behavioral responses to free fatty acids (FFAs), the building blocks of fats, rather than on neural coding of FFAs. The gustatory chorda tympani nerve (CT) has been implicated in FFA detection, as bilateral transection of the CT (CTX) significantly impairs the discrimination of linoleic acid (LA), a polvunsaturated free fatty acid and main component of some kinds of dietary fat (Stratford et al., 2006). Yet, the CT is unresponsive to lingual application of LA. Thus, a paradox exists and the exact role of the CT in LA taste discrimination remains unknown. This is particularly pertinent because an understanding of the mechanisms involved in fatty acid perception can provide insight into the development of obesity. The following experiments are designed to determine the role of the CT in LA gustatory responses using parallel behavioral and electrophvsiological methods. Because CTX disrupts:neural control of salivary secretion, Specific Aim 1 will determine the contribution of the salivary glands and salivary sodium concentration specifically to fat taste. Moreover, because fat is traditionally considered an enhancer for other tastes, Specific Aim 1 will also test the hypothesis that the addition of LA will modulate CT electrophysiological activity to other taste stimuli. In fact, LA may require a background of saliva (dilute saline) to activate taste cells (i.e., taste cells are incapable of responding to LA unless there is some low level of sodium in the environment). This would explain, in part, the discrepancy between my behavioral data (in which saliva is present) and CT electrophysiological data (in which salivary sodium is rinsed off during water rinses). Changes in CT responses to taste stimuli when LA is added would suggest that LA modulates CT responses to other taste stimuli. Finally, CTX does not abolish LA detection, suggesting that other gustatory nerves may also be involved. Specific Aim 2 will determine the role of peripheral gustatory nerves in LA taste using a conditioned taste aversion protocol with gustatory nerve transections. Impairment of LA taste discrimination following a specific gustatory nerve transection will implicate that gustatory nerve in LA taste detection. Thus, these data provide insight into the role of fat taste in the development of obesity.