Neural Basis of Behavioral Plasticity in a Simple System

描述（由申请人提供）：我们研究的长期目标是 表征赋予生物体产生能力的机制 行为是可塑的，因为它可以不断修改， 适应外部环境的变化。我们的实验是 在具有实验上有利的特征的相对简单的模型系统中。 在这个系统中，当高阶命令/调节神经元 都被激活了当食物接触到一个 动物和激活感觉神经元。一些食物引起的改变， 进食与感觉神经元的活动一致， 发生在感觉神经元不再活跃之后，即，他们依赖于一个？记忆？ 的刺激。在上一个资助期，我的实验室发现了 由食物激活的神经元，启动从咬到吞的转变。 本申请中描述的工作是对最近一项令人兴奋的发现的后续研究 关于如何传入引起的变化，喂养可能会发生。也就是说， 我们的数据表明，传入输入只修改运动活动， ?门入？如果传入神经在静止的动物中被激活， 将不会生成输出。相反，当传入神经被激活时， 行为是持续的，喂养动作可以改变。传入输入是， 然而，仅在特定时间内才能进入。这种布置允许 传入诱导的行为改变，但不允许传入诱导的 行为的重组。本提案中描述的实验将 确定这种传入传递的调节是如何发生的。我们将测试 一个特定的假设，假设门控至少部分地由 选择性控制感觉神经元中的尖峰传播。我们将描述 细胞机制，我们将进行实验， 半完整的准备工作，将细胞的发现与行为。我们 我相信我们的工作将为神经系统的功能障碍提供深入的了解。 与注意力缺陷有关的系统。数据显示，至少 在某些情况下（例如，在精神分裂症中）这些功能障碍特别是 与感觉门控缺陷有关

DESCRIPTION (provided by applicant): The long term goal of our research is to characterize mechanisms that endow an organism with its ability to generate behavior that is plastic in the sense that it can be continuously modified to accommodate changes in the external environment. Our experiments are conducted in a relatively simple model system with experimentally advantageous features. In this system biting is generated when higher order command/modulatory neurons are activated. Bites are converted into bite-swallows when food contacts an animal and activates sensory neurons. Some of the food-induced alterations in feeding are coincident with activity in sensory neurons while other alterations occur after sensory neurons are no longer active, i.e., they rely on a ?memory? of the stimulus. In the previous grant period my laboratory identified sensory neurons activated by food that initiate bite to bite-swallow transformations. Work described in this application follows up on an exciting recent finding concerning how afferent-induced changes in feeding are likely to occur. Namely, our data suggest that afferent input only modifies motor activity if it is ?gated-in?. If afferents are activated in quiescent animals, reflex or motor output will not be generated. In contrast, when afferents are activated while behavior is ongoing, feeding movements can be altered. Afferent input is, however, only gated-in at certain times. This arrangement permits afferent-induced modifications of behavior but does not permit afferent-induced reconfigurations of behavior. Experiments described in this proposal will determine how this regulation of afferent transmission occurs. We will test a specific hypothesis that postulates that gating occurs at least in part by the selective control of spike propagation in sensory neurons. We will characterize cellular mechanisms that are utilized and we will conduct experiments in semi-intact preparations that will relate cellular findings to behavior. We believe that our work will provide insights into dysfunctions of the nervous system that are associated with attention deficits. Data indicate that at least in some cases (e.g., in schizophrenia) these dysfunctions are specifically associated with defects in sensory gating.