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中文摘要
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项目总结 朝日实验室的首要目标是了解动物通过神经遗传学机制-- 以一种依赖于上下文的方式在社交行为中采取公正的策略。为此,他们研究了激励性交互作用-- 果蝇与黑腹果蝇之间的相互作用。苍蝇在不同类型和强度的社交活动中做出选择 基于内部和外部条件的行为(例如,喂食状态、交配状态、预繁殖的结果 明显的交互)。高精度操纵果蝇基因和神经元功能的有力工具 Sion为理解这种丰富的行为背后的神经遗传机制提供了一个独特的平台 灵活性。Asahina实验室在过去4年中的一个主要发现是,章鱼胺的一个特定子集- 能神经元抑制攻击,转录调节神经控制着 这些神经元发挥攻击性“刹车”功能所需的基因。他们还描述了基因 三种男性特有的攻击促进神经元之间功能差异的来源。有能力 以基因控制先前特征的攻击促进神经元及其新的发展 以精细分辨率描述激励性相互作用的计算方法,朝日的目标 未来五年的实验室任务是:1)阐明动物如何建立基于 根据经验,以及2)表征神经元和遗传机制,通过这些机制导致特定营养物质的缺乏 在食物竞争中调整行为策略。第一个目标将通过在他们的基础上 最近的研究发现,支配-服从关系可以超越实验性的攻击激活-- 促进神经元。他们将测试这一预测,即依赖经验的攻击行为调制- IORS是由一种未被描述的神经元或分子机制实现的。第二个目标的灵感来自 他们发现,缺乏氨基酸会显著增加雄性和雌性果蝇的攻击性,但 只有当环境中存在活的酵母时。他们将阐明特定的营养赤字是如何改变 攻击性控制神经元和遗传模块的功能。这些研究建立在实验室的优势之上 在遗传学和高级行为量化方面,再加上他们在开发新的行为异常方面的独创性 解决动物行为领域长期存在的问题的摘录,最重要的是:动物是如何 从战略上在行为选项之间做出选择?理论分析预测,动物一定有 发展了复杂的机制,以集成信息并计算与 在竞技性互动过程中的特殊行为。然而,实验系统要定量地表征 这些行为选择的神经基础仍然难以捉摸。拟议中的实验提供了进入 从成本/成本角度重新定义基因和神经元的功能,解决这一问题的要点-- 比赛过程中的效益计算。拟议的研究将通过说明运营情况来弥补这一关键差距 基因和神经元控制社会行为的上下文相关调节的原理。
英文摘要
PROJECT SUMMARY The overarching goal of the Asahina lab is to understand the neurogenetic mechanisms by which animals ad- just tactics during social behaviors in a context-dependent manner. To this end, they study agonistic interac- tions between Drosophila melanogaster fruit flies. Flies choose between different types and intensities of social behaviors based on both internal and external conditions (e.g., feeding status, mating status, outcomes of pre- vious interactions). Powerful tools for manipulating gene and neuronal function in Drosophila with high preci- sion provides a unique platform for understanding the neurogenetic mechanisms underlying this rich behavioral flexibility. One major finding from the Asahina lab during the past 4 years is that a specific subset of octopamin- ergic neurons suppress aggression, and that the transcriptional regulator nervy controls the expression of genes necessary for these neurons to function as an aggression “brake”. They also characterized the genetic origins of the functional differences between three male-specific aggression-promoting neurons. With the ability to genetically control previously characterized aggression-promoting neurons and their development of novel computational methodologies for characterizing agonistic interactions at fine resolution, goals of the Asahina lab over the next five years are to: 1) elucidate how animals establish dominant-submissive hierarchies based on experience, and 2) characterize the neuronal and genetic mechanisms by which deficits in specific nutrients modulate behavioral tactics during competition for food. The first goal will be pursued by building upon their recent finding that the dominant-submissive relationship can override experimental activation of aggression- promoting neurons. They will test the prediction that experience-dependent modulation of aggressive behav- iors is implemented by an uncharacterized neuronal or molecular mechanism. The second goal is inspired by their finding that amino-acid deprivation dramatically increases aggression in both male and female flies, but only when live yeast is present in the environment. They will elucidate how specific nutrition deficits alter the function of aggression-controlling neuronal and genetic modules. These studies build upon strengths of the lab in genetics and advanced behavioral quantification, plus their ingenuity in developing novel behavioral para- digms for addressing longstanding questions in the field of animal behavior, most importantly: how do animals strategically choose between behavioral options? Theoretical analyses have predicted that animals must have evolved sophisticated mechanisms to integrate information and calculate costs and benefits associated with a particular behavior during agonistic interactions. However, experimental systems to quantitatively characterize the neural bases of these behavioral choices have remained elusive. The proposed experiments provide entry points for solving this problem by re-defining functions of genes and neurons from the perspective of cost/ben- efit calculations during competition. Proposed research will bridge this critical gap by illuminating operational principles by which genes and neurons control context-dependent adjustment of social behaviors.
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Peptidergic neuromodulation of microcircuits that control chemosensation-induced behaviors
Peptidergic neuromodulation of microcircuits that control chemosensation-induced behaviors
Peptidergic neuromodulation of microcircuits that control chemosensation-induced behaviors
Peptidergic neuromodulation of microcircuits that control chemosensation-induced behaviors
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