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Kirszenblat, L.

Publications and source records attributed to Kirszenblat, L..

4 recordsLinked to original sources

Sleep promotes aversive value coding in Drosophila

Sleep is a state of reduced behavioural responsiveness to the external world. Lowered arousal is thought to arise from sensory gating in the brain, yet there is compelling evidence that stimuli can still be processed to some degree. Which aspects of sensory information are processed during sleep remains largely unknown. Here, we perform comprehensive recordings of activity from multiple neuron types during sleep and wakefulness in the Drosophila olfactory association center. We find that baseline activity of dopamine neurons (DANs) is distinct between active, rest and sleep states, enabling a decoder to predict when the fly is asleep. Optogenetic inhibition of DANs acutely induces sleep and lowers odor-evoked arousal, suggesting causality between DAN activity and behavior. We then examine odor processing during sleep, and find that whereas coding of odor identity in Kenyon cells (KCs) remains intact, coding of odor value in DANs is altered. Specifically, DANs encoding positive (attractive) and negative (aversive) values change their odor responses in an opposing manner, producing more aversive odor representations during sleep. Consistent with these changes in neural activity, sleeping flies awoken by odors show reduced approach and increased avoidance behaviour. Taken together, our data reveal that the brain does not simply suppress the propagation of sensory signals during sleep; rather, it utilizes different cell types to retain or modify specific aspects of sensory information. The aversive odor evaluation in DANs may have ethological benefits as it suppresses the motivation to pursue attractive odors during sleep and primes defensive action when aroused by the scent of potential dangers.

neuroscience↗

A conserved role for sleep in supporting spatial learning in Drosophila

Sleep loss and aging impair hippocampus-dependent spatial learning in mammalian systems. Here we use the fly Drosophila melanogaster to investigate the relationship between sleep and spatial learning in healthy and impaired flies. The spatial learning assay is modeled after the Morris Water Maze. The assay uses a thermal maze consisting of a 5x5 grid of Peltier plates maintained at 36-37{degrees}C and a visual panorama. The first trial begins when a single tile that is associated with a specific visual cue is cooled to 25{degrees}C. For subsequent trials, the cold tile is heated, the visual panorama is rotated and the flies must find the new cold-tile by remembering its association with the visual cue. Significant learning was observed with two different wild-type strains - Cs and 2U, validating our design. Sleep deprivation prior to training impaired spatial learning. Learning was also impaired in the classic learning mutant rutabaga (rut); enhancing sleep restored learning to rut mutants. Further we found that flies exhibited dramatic age-dependent cognitive decline in spatial learning starting at 20-24 days of age. These impairments could be reversed by enhancing sleep. Finally, we find that spatial learning requires dopaminergic signaling and that enhancing dopaminergic signaling in aged flies restored learning. Our results are consistent with the impairments seen in rodents and humans. These results thus demonstrate a critical conserved role for sleep in supporting spatial learning, and suggest potential avenues for therapeutic intervention during aging. STATEMENT OF SIGNIFICANCEWe have studied the relationship between sleep and plasticity using a Drosophila learning assay modified after the Morris Water Maze. Using this assay, we find that sleep loss impairs spatial learning. As in mammals, flies exhibited age-dependent spatial learning impairments. Importantly, the age-dependent impairments were reversed by enhancing sleep. Interestingly, our results mirror studies on hippocampus dependent memories in rodents and humans. Thus, our data describe an evolutionarily conserved role for sleep in regulating spatial learning. They also support augmenting sleep as a therapeutic strategy to ameliorate learning impairments.

neuroscience↗

{-}{-} Downregulation of a satiety signal from peripheral fat bodies improves visual attention while reducing sleep need in Drosophila .

Sleep is vital for survival. Yet, under environmentally challenging conditions such as starvation, animals suppress their need for sleep. Interestingly, starvation-induced sleep loss does not evoke a subsequent sleep rebound. Little is known about how starvation-induced sleep deprivation differs from other types of sleep loss, or why some sleep functions become dispensable during starvation. Here we demonstrate that downregulation of unpaired-2 (upd2, the Drosophila ortholog of leptin), is sufficient to mimic a starved-like state in flies. We use this genetically starved state to investigate the consequences of a starvation signal on visual attention and sleep in otherwise well-fed flies, thereby sidestepping the negative side-effects of undernourishment. We find that knockdown of upd2 in the fat body is sufficient to suppress sleep while also increasing selective visual attention and promoting night-time feeding. Further, we show that this peripheral signal is integrated in the fly brain via insulin-expressing cells. Together, these findings identify a role for peripheral tissue-to-brain interactions in the simultaneous regulation of sleep and attention, to potentially promote adaptive behaviors necessary for survival in hungry animals.\n\nAuthor SummarySleep is important for maintaining both physiological (e.g., metabolic, immunological, and developmental) and cognitive processes, such as selective attention. Under nutritionally impoverished conditions, animals suppress sleep and increase foraging to locate food. Yet it is currently unknown how an animal is able to maintain well-tuned cognitive processes, despite being sleep deprived. Here we investigate this question by studying flies that have been genetically engineered to lack a satiety signal, and find that signaling from fat bodies in the periphery to insulin-expressing cells in the brain simultaneously regulates sleep need and attention-like processes.

neuroscience↗

Sleep regulates visual selective attention in Drosophila

Although sleep-deprivation is known to impair attention in humans and other mammals, the underlying reasons are not well understood, and whether similar effects are present in non-mammalian species is not known. We therefore sought to investigate whether sleep is important for optimising attention in an invertebrate species, the genetic model Drosophila melanogaster. We developed a high-throughput paradigm to measure visual attention in freely-walking Drosophila, using competing foreground/background visual stimuli. We found that whereas sleep-deprived flies could respond normally to either stimulus alone, they were more distracted by background cues in a visual competition task. Other stressful manipulations such as starvation, heat exposure, and mechanical stress had no effects on visual attention in this paradigm. In contrast to sleep-deprivation, providing additional sleep using the GABA-A agonist 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol (THIP) did not affect attention in wild-type flies, but significantly improved attention in the learning mutant dunce. Our results reveal a key function of sleep in optimising attention processes in Drosophila, and establish a behavioural paradigm that can be used to explore the molecular mechanisms involved.\n\nSummary statementSleep deprivation specifically impairs visual selective attention in fruit flies, without affecting behavioural responses to simple visual stimuli.

animal behavior and cognition↗