State-dependent modulation of taste and temperature integration in Drosophila

动物不断地检测不同的环境刺激并改变它们的行为或行为。 基于他们的内部状态。动物如何整合外部多种感官信息， 其内部状态基本上不清楚。 这项提案的具体目标是探索内部状态的神经回路和机制- 多种感觉整合的依赖性调节。我们将利用一个强大的，多功能的， 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 最近确定了一种新的头相反应（CPR）引起的味觉温度整合。CPR是 从饥饿状态快速和部分恢复，并且是许多动物的稳健和典型反应， 包括人类当动物饥饿时，对食物的感官检测会激发动物的生理反应。 这种快速反应就是心肺复苏术我们的初步数据表明， 整合导致果蝇的CPR。 在这个R34应用中，我们将探索如何通过使用CPR来调节味觉-温度整合， 输出.我们将通过监测味觉和体温来研究味觉-体温整合的神经机制。 温度处理神经元活动使用钙成像。此外，饥饿信号，如 果蝇神经肽F是哺乳动物神经肽Y的同系物，对CPR至关重要，这表明， 饥饿信号调节味觉-温度神经回路。这些初步的数据导致我们的中央 饥饿信号调节味觉和温度处理之间的感觉整合 神经元，它驱动心肺复苏术。提出了以下两个具体目标：在目标1中，我们将探索神经 味温一体化的机理和电路。在目标2中，我们将探讨 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.