Animals always seek rewards and the related neural basis has been well studied. However, what happens when animals fail to get a reward is largely unknown, although this is commonly seen in behaviors such as predation. Here, we set up a behavioral model of repeated failure in reward pursuit (RFRP) in Drosophila larvae. In this model, the larvae were repeatedly prevented from reaching attractants such as yeast and butyl acetate, before finally abandoning further attempts. After giving up, they usually showed a decreased locomotor speed and impaired performance in light avoidance and sugar preference, which were named as phenotypes of RFRP states. In larvae that had developed RFRP phenotypes, the octopamine concentration was greatly elevated, while tβh mutants devoid of octopamine were less likely to develop RFRP phenotypes, and octopamine feeding efficiently restored such defects. By down-regulating tβh in different groups of neurons and imaging neuronal activity, neurons that regulated the development of RFRP states and the behavioral exhibition of RFRP phenotypes were mapped to a small subgroup of non-glutamatergic and glutamatergic octopaminergic neurons in the central larval brain. Our results establish a model for investigating the effect of depriving an expected reward in Drosophila and provide a simplified framework for the associated neural basis.Electronic supplementary materialThe online version of this article (10.1007/s12264-018-0248-0) contains supplementary material, which is available to authorized users.
Sleep is regulated by environmental factors including temperature, but the neural circuits that receive the sensory signal and mediate the regulation remain unclear. We examined how cold could influence Drosophila sleep patterns and its neural mechanism. The results showed that Drosophila has more sleep duration, less sleep latency and deeper sleep depth under cold condition. We identified the Insulin-producing Cells (IPCs) can be activated by cold, and receive the cold signal from the 11216 cold-sensing neuron without a direct synaptic connection. Elevation of IPCs' sensitivity to cold impairs the sleeppromoting effect of cold while blocking of IPCs enhance the effect mostly on sleep circadian, suggesting that the cold activated IPCs have a compensative role in sleep regulation. Our finding revealed a potential neural circuit that help maintain sleep circadian in detrimental environment and may give new insight to the complicated sleep regulation mechanism.
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