The fruit fly, Drosophila melanogaster, is able to discriminate visual landmarks and form visual long-term memory in a flight simulator. Studies focused on the molecular mechanism of long-term memory have shown that memory formation requires mRNA transcription and protein synthesis. However, little is known about the molecular mechanisms underlying the visual learning paradigm. The present study demonstrated that both spaced training procedure (STP) and consecutive training procedure (CTP) would induce long-term memory at 12 hour after training, and STP caused significantly higher 12-h memory scores compared with CTP. Label-free quantification of liquid chromatography-tandem mass spectrometry (LC-MS/MS) and microarray were utilized to analyze proteomic and transcriptomic differences between the STP and CTP groups. Proteomic analysis revealed 30 up-regulated and 27 down-regulated proteins; Transcriptomic analysis revealed 145 up-regulated and 129 down-regulated genes. Among them, five candidate genes were verified by quantitative PCR, which revealed results similar to microarray. These results provide insight into the molecular components influencing visual long-term memory and facilitate further studies on the roles of identified genes in memory formation.
Animals ; Conditioning (Psychology) ; physiology ; Drosophila Proteins ; genetics ; metabolism ; Drosophila melanogaster ; genetics ; metabolism ; physiology ; Flight, Animal ; physiology ; Gene Expression Profiling ; methods ; Memory ; physiology ; Oligonucleotide Array Sequence Analysis ; Proteomics ; methods ; Time Factors ; Vision, Ocular ; physiology

In the original publication the fifth line starting with "… with circa 1000, 1000 neurons?" in section Concluding Remarks and Perspectives is incorrectly published. The correct text should read "… with circa 100, 000 neurons?"

Nervous systems endow animals with cognition and behavior. To understand how nervous systems control behavior, neural circuits mediating distinct functions need to be identified and characterized. With superior genetic manipulability, Drosophila is a model organism at the leading edge of neural circuit analysis. We briefly introduce the state-of-the-art genetic tools that permit precise labeling of neurons and their interconnectivity and investigating what is happening in the brain of a behaving animal and manipulating neurons to determine how behaviors are affected. Brain-wide wiring diagrams, created by light and electron microscopy, bring neural circuit analysis to a new level and scale. Studies enabled by these tools advances our understanding of the nervous system in relation to cognition and behavior.

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.
Acetates ; pharmacology ; Animals ; Animals, Genetically Modified ; Avoidance Learning ; physiology ; Biogenic Amines ; metabolism ; Conditioning, Operant ; physiology ; Drosophila ; physiology ; Drosophila Proteins ; genetics ; metabolism ; Feeding Behavior ; drug effects ; physiology ; Instinct ; Larva ; physiology ; Locomotion ; drug effects ; genetics ; Nervous System ; cytology ; Neurons ; physiology ; Octopamine ; metabolism ; RNA Interference ; physiology ; Reward ; Statistics, Nonparametric ; Transcription Factors ; genetics ; metabolism

When facing a sudden danger or aversive condition while engaged in on-going forward motion, animals transiently slow down and make a turn to escape. The neural mechanisms underlying stimulation-induced deceleration in avoidance behavior are largely unknown. Here, we report that in Drosophila larvae, light-induced deceleration was commanded by a continuous neural pathway that included prothoracicotropic hormone neurons, eclosion hormone neurons, and tyrosine decarboxylase 2 motor neurons (the PET pathway). Inhibiting neurons in the PET pathway led to defects in light-avoidance due to insufficient deceleration and head casting. On the other hand, activation of PET pathway neurons specifically caused immediate deceleration in larval locomotion. Our findings reveal a neural substrate for the emergent deceleration response and provide a new understanding of the relationship between behavioral modules in animal avoidance responses.