State-dependent modulation of taste and temperature integration in Drosophila

项目摘要：动物不断检测到不同的环境刺激并改变它们的行为或 基于他们的内在状态的生理学。动物如何将外部的多种感觉信息与 内部状况在很大程度上尚不清楚。 这项提议的具体目标是探索内部状态的神经回路和机制- 对多种感觉整合的依赖调节。我们将利用一个强大的、多功能的和相对 简单的遗传模型，果蝇，以解决味觉-温度整合的神经机制。我们 最近发现了一种新的头位相反应(CPR)，它是由味觉-温度整合引起的。心肺复苏术 从饥饿状态中迅速和部分恢复，对许多动物来说是强有力的和典型的反应， 包括人类。当动物饥饿时，对食物的感官检测会引起生理上的突发反应。 他们身体的变化；这种快速反应就是CPR。我们的初步数据表明，味觉-温度 整合导致了苍蝇的CPR。 在R34应用程序中，我们将探索如何通过使用CPR AS来调节味温整合 输出。我们将通过监测味觉和温度来研究味觉-温度整合的神经机制 使用钙成像技术对神经元活动进行温度处理。此外，饥饿的信号，如 果蝇神经肽F是哺乳动物神经肽Y的同源物，对CPR至关重要，这表明 饥饿信号调节着味觉-温度神经回路。这些初步数据导致我们的中央 假设：饥饿信号调节味觉和温度加工之间的感觉整合 神经元，驱动心肺复苏术。提出了以下两个具体目标：在目标1中，我们将探索神经 味觉-温度整合的机制和回路。在目标2中，我们将探索通过哪些机制 内部状态调节味觉-温度整合。

PROJECT SUMMARY: Animals constantly detect different environmental stimuli and change their behavior or physiology based on their internal state. How animals integrate the external multiple sensory information with the internal state is largely unclear. The specific goal of this proposal is to explore the neural circuits and mechanisms of internal state- dependent modulation of multiple sensory integrations. We will draw on a powerful, versatile, and relatively simple genetic model, Drosophila, to address the neural mechanisms of taste-temperature integration. We recently identified a new cephalic phase response (CPR) caused by taste-temperature integration. CPR is rapid and partial recovery from the starved state and is a robust and typical response for many animals, including humans. When animals are hungry, the sensory detection of food elicits bursts of physiological changes in their bodies; this rapid response is CPR. Our primary data suggest that taste-temperature integration leads to CPR in flies. In this R34 application, we will explore how taste-temperature integration is regulated by using CPR as output. We will examine neural mechanisms of taste-temperature integration by monitoring taste- and temperature-processing neuronal activity using calcium imaging. Furthermore, hunger signals such as Drosophila neuropeptide F, a homolog of mammalian neuropeptide Y, are critical for CPR, suggesting that hunger signals modulate the taste-temperature neural circuits. These preliminary data lead to our central hypothesis: hunger signals modulate the sensory integration between taste- and temperature-processing neurons, which drives CPR. The following two specific aims are proposed: In Aim 1, we will explore the neural mechanisms and circuits of taste-temperature integration. In Aim 2, we will explore the mechanisms by which the internal state modulates taste-temperature integration.