DIET-INDUCED PLASTICITY IN TASTE CELLS MODIFIES FEEDING

所有动物都能适应不断变化的环境。这背后的一个关键特征是 适应的过程是感官的可塑性，它涵盖的范围很广 来自反应性变化的现象(习惯化和 敏感化)到更复杂形式的联想学习。这 提案描述了检验饮食诱导的可塑性的实验 味觉细胞，以及这种可塑性如何在 重要的神经生物学模型--六色毛虫。这 人们普遍对这一现象感兴趣，因为经验诱导的可塑性 化学感觉系统的一个普遍但鲜为人知的特征，以及 它为研究复合体的生物学基础提供了一种工具 行为：偏爱食物。重点将放在苦味上，因为 它在毒物检测中的重要性。初步实验已经 证明了两天的饮食暴露在苦味中 (咖啡因)会导致响应性大幅下降(即， 对苦味敏感的味觉细胞(或苦味细胞) 咖啡因。此外，苦味细胞的脱敏与 对咖啡因饮食的味觉习惯。这些结果 是用一种使人能够重复进行的准备来收集的 单一味觉细胞刺激前后的电生理记录 饮食控制在不同毛毛虫之间进行比较 使用同源味觉细胞，并将脱敏与进食联系起来 同一种动物的行为。基于这些实验，以下是 制定了具体目标：(I)确定长期接触 任何刺激苦味细胞的味道都会产生这两种味道 对同一品尝者脱敏和味觉习惯(Ii) 确定对一种苦味的脱敏和味觉习惯性 Tastant推广到其他苦味，(Iii)确定是否 对不同苦味的脱敏反应是通过 共同的机制，以及(Iv)确定脱敏是否 由作用于味觉细胞的苦味化合物控制 系统地通过血液，直接在没有摄入的情况下，或者 间接地通过离心式神经传出。希望这一天 拟议中的研究将揭示味觉感受器系统的一些基本情况 这将推广到人类。这样的概括可以提供新的 对人类饮食和食物偏好之间相互作用的洞察， 以及这种相互作用可能如何导致饮食失调。更好的 对进食苦味与苦味关系的认识 敏感度也有助于解释有毒物质的高摄入率 人类使用的家用物质。

All animals adapt to changing environments. A key feature underlying this adaptation process is sensory plasticity, which encompasses a broad range of phenomena from alterations in responsiveness (habituation and sensitization) to more complex forms of associative learning. This proposal describes experiments that examine diet-induced plasticity in taste cells, and how this plasticity produces gustatory habituation in an important neurobiological model, Manduca sexta caterpillars. This phenomenon is of general interest because experience-induced plasticity is a prevalent, but poorly understood, feature of chemosensory systems, and it provides a tool with which to study the biological basis of a complex behavior: food preference. The focus will be on bitter taste because of its importance in poison detection. Preliminary experiments have demonstrated that two days of dietary exposure to a bitter tastant (caffeine) causes a large decrease in responsiveness (i.e., desensitization) of the bitter-sensitive taste cell (or bitter cell) to caffeine. Further, the desensitization of the bitter cell was associated with gustatory habituation to a diet treated with caffeine. These results were collected with a preparation that enables one to make repeated electrophysiological recordings from single taste cells before and after dietary manipulations make comparisons across individual caterpillars using homologous taste cells, and relate desensitization to feeding behavior in the same animal. Based on these experiments, the following specific aims were devised: (i) to determine whether prolonged exposure to any tastant that stimulates the bitter cell will produce both desensitization and gustatory habituation to that same tastant' (ii) to determine whether desensitization and gustatory habituation to one bitter tastant generalize to other bitter tastants, (iii) to determine whether the desensitization response to different bitter tastants is mediated by a common mechanism, and (iv) to determine whether desensitization is controlled by bitter compounds acting on the taste cells either systemically via the blood, directly in the absence of ingestion, or indirectly through centrifugal neural efferents. It is hoped that the proposed studies will reveal something basic about taste receptor systems that will generalize to humans. Such generalizations could provide new insights into the interaction between diet and food preference in humans, and how this interaction may contribute to eating disorders. A better understanding of the connection between intake of bitter foods and bitter sensitivity could also help explain the high rate of ingestion of toxic household substances by humans.