Presynaptic Gain Control Drives Sweet and Bitter Taste Integration in Drosophila
Presynaptic Gain Control Drives Sweet and Bitter Taste Integration in Drosophila
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DOI：
10.1016/j.cub.2014.07.020
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发表时间：
2014-09-08
期刊：
影响因子：
9.2
通讯作者：
Gordon, Michael D.
中科院分区：
文献类型：
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作者：
Chu, Bonnie;Chui, Vincent;Gordon, Michael D.
味觉对于确定食物的营养适宜性至关重要。甜味和苦味是哺乳动物的主要味觉方式，它们在果蝇中的行为相关性相似。甜味促进对能量来源的食欲反应，而苦味则促进避免潜在毒素并抑制甜味反应 [1, 2]。尽管它们对生存很重要，但人们对甜味和苦味整合背后的神经回路机制知之甚少。在这里，我们描述了果蝇的突触前增益控制机制，该机制对甜味和苦味通道产生不同的影响，并介导这些相反刺激的整合。众所周知，增益控制在果蝇嗅觉中发挥着重要作用，其中 GABA(B) 受体 (GABA(B)R) 介导感觉神经元输出的球内和球间突触前抑制 [3-5]。在味觉系统中，我们发现对甜味化合物做出反应的味觉受体神经元 (GRN) 表达 GABA(B)R，而对苦味做出反应的味觉受体神经元则不表达 GABA(B)R。 GABA(B)R 介导甜味 GRN 中钙反应的突触前抑制，甜味和苦味刺激都会引起 GABA 神经元在 GRN 轴突末端附近的活动。 GABA(B)R 的药理学封锁和遗传减少都会导致糖反应增加，并减少苦味化合物对甜味反应的抑制。我们提出了一种模型，其中 GABA 通过 GABA(B)R 发挥作用，通过突触前增益控制扩大甜味 GRN 的动态范围，并在存在相反苦味刺激的情况下抑制甜味 GRN 的输出。
The sense of taste is critical in determining the nutritional suitability of foods. Sweet and bitter are primary taste modalities in mammals, and their behavioral relevance is similar in flies. Sweet taste drives the appetitive response to energy sources, whereas bitter taste drives avoidance of potential toxins and also suppresses the sweet response [1, 2]. Despite their importance to survival, little is known about the neural circuit mechanisms underlying integration of sweet and bitter taste. Here, we describe a presynaptic gain control mechanism in Drosophila that differentially affects sweet and bitter taste channels and mediates integration of these opposing stimuli. Gain control is known to play an important role in fly olfaction, where GABA(B) receptor (GABA(B)R) mediates intra- and interglomerular presynaptic inhibition of sensory neuron output [3-5]. In the taste system, we find that gustatory receptor neurons (GRNs) responding to sweet compounds express GABA(B)R, whereas those that respond to bitter do not. GABA(B)R mediates presynaptic inhibition of calcium responses in sweet GRNs, and both sweet and bitter stimuli evoke GABAergic neuron activity in the vicinity of GRN axon terminals. Pharmacological blockade and genetic reduction of GABA(B)R both lead to increased sugar responses and decreased suppression of the sweet response by bitter compounds. We propose a model in which GABA acts via GABA(B)R to expand the dynamic range of sweet GRNs through presynaptic gain control and suppress the output of sweet GRNs in the presence of opposing bitter stimuli.