DIET-INDUCED PLASTICITY IN TASTE CELLS MODIFIES FEEDING

饮食引起的味觉细胞可塑性改变了进食

基本信息

批准号：
2733681
负责人：
JOHN I GLENDINNING
金额：
$ 8.62万
依托单位：
BARNARD COLLEGE
依托单位国家：
美国
项目类别：
财政年份：
1994
资助国家：
美国
起止时间：
1994-07-01 至 2000-06-30
项目状态：
已结题

项目摘要

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.

所有动物都适合不断变化的环境。此基础的关键功能适应过程是感觉可塑性，它包含广泛的范围反应性改变（习惯和敏化）对更复杂的联想学习形式。这提案描述了检查饮食引起的可塑性的实验味道细胞，以及这种可塑性如何在重要的神经生物学模型，曼达卡·塞克斯塔毛毛虫。这现象是普遍关注的，因为经验引起的可塑性是化学感应系统的普遍但知之甚少的特征，它提供了一种研究复杂的生物学基础的工具行为：食物偏爱。重点将放在苦味上它在毒物检测中的重要性。初步实验具有证明了两天的饮食暴露于苦味（咖啡因）导致反应性大大降低（即对苦敏感细胞（或苦细胞）的脱敏）咖啡因。此外，苦细胞的脱敏是相关的伴有咖啡因治疗的饮食的味道习惯。这些结果收集一项准备工作，使一个人能够重复来自单个味觉细胞之前和之后的电生理记录饮食中的操纵使人比较单个毛毛虫使用同源味道细胞，并将脱敏与进食相关联同一动物的行为。基于这些实验，以下设计了具体目标：（i）确定是否长时间接触任何刺激苦细胞的味道都会产生脱敏和对同一味道的敏感性和味道习惯”（ii）确定脱敏和味道习惯是否对一个痛苦味道剂对其他苦味剂进行概括，（iii）确定是否是否对不同苦味剂的脱敏反应是由一种常见的机制，（iv）确定脱敏是否为由作用在味道细胞上的苦味化合物控制直接在没有摄入的情况下通过血液进行系统地。间接通过离心神经传出。希望拟议的研究将揭示有关味觉受体系统的基本内容这将概括为人类。这样的概括可以提供新的洞悉饮食与人类食品偏好之间的相互作用，以及这种相互作用如何导致饮食失调。更好理解苦味和苦味的摄入量之间的联系敏感性还可以帮助解释有毒的高摄入率人类的家用物质。