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Artiushin, G.

Publications and source records attributed to Artiushin, G..

3 recordsLinked to original sources

A three-dimensional immunofluorescence atlas of the brain of the hackled-orb weaver spider, Uloborus diversus.

Spider orb-web building is a captivating, rare example of animal construction, whose neural underpinnings remain undiscovered. We created a three-dimensional atlas for the hackled orb-weaver, Uloborus diversus, based on immunostaining for the presynaptic component, synapsin, in whole-mounted spider synganglia. Whereas spider neuroanatomy has thus far been most comprehensively studied in cursorial species, this optically-sectioned atlas contributes a continuous, finely resolved model of the central nervous system of an orb-web building spider. Aligned to this volume, we examined the expression patterns of neuronal populations representing many of the classical neurotransmitters and neuromodulators (GABA, Acetylcholine, Serotonin, Octopamine/Tyramine), as well as a subset of neuropeptides (AllatostatinA, Crustacean Cardioactive Peptide (CCAP), FMRFamide, Proctolin) - detailing immunoreactivity in an unbiased fashion throughout the synganglion to reveal co-expression in known structures (such as the arcuate body), as well as novel neuropils not readily apparent in prior spider research, including the tonsillar neuropil as well as a potential protocerebral bridge. These structures provide targets for future functional studies, and taken together could represent a spider equivalent of the central complex, contributing to behaviors such as web-building.

neuroscience↗

Modulation of sleep by trafficking of lipids through the Drosophila blood brain barrier

Endocytosis through Drosophila glia is a significant determinant of sleep amount and occurs preferentially during sleep in glia of the blood brain barrier (BBB). To identify metabolites whose trafficking is mediated by sleep-dependent endocytosis, we conducted metabolomic analysis of flies that have increased sleep due to a block in glial endocytosis. We report that acylcarnitines, molecules that conjugate with long chain fatty acids to promote their transport, accumulate in heads of these animals. In parallel, to identify transporters and receptors whose loss contributes to the sleep phenotype caused by blocked endocytosis, we screened genes enriched in barrier glia for effects on sleep. We find that knockdown of lipid transporters LRP1&2 as well as carnitine transporters ORCT1&2 increases sleep. In support of the idea that the block in endocytosis affects trafficking through specific transporters, knockdown of LRP or ORCT transporters also increases acylcarnitines in heads. We propose that lipid species, such as acylcarnitines, are trafficked through the BBB via sleep-dependent endocytosis, and their accumulation in the brain increases the need for sleep.

neuroscience↗

AANAT1 functions in astrocytes to regulate sleep homeostasis.

Characteristic features of sleep are conserved among species [1], and from humans to insects sleep is influenced by neural circuits involving monoamines such as serotonin and dopamine [2]. Glial cells have been increasingly implicated in mechanisms of baseline and homeostatic sleep regulation in mammals and flies [3-11], but it remains unknown whether and how glia might influence monoaminergic control of sleep. Sleep is regulated by circadian rhythms and a homeostatic drive to compensate for prolonged wakefulness, and growing evidence suggests that neural mechanisms controlling homeostatic sleep can be discriminated from those controlling baseline sleep [12-15]. In Drosophila, mutants of arylalkylamine N-acetyltransferase 1 (AANAT1lo) have normal baseline amounts of sleep and motor activity, but increased rebound sleep following deprivation [16]. AANAT1 can acetylate and inactivate monoamines in vitro [17], but the role of AANAT1 in vivo remains poorly understood. We find AANAT1 to be expressed in astrocytes and subsets of neurons in the adult Drosophila brain, with levels in astrocytes declining markedly overnight. In sleep-deprived AANAT1 mutant flies, heightened rebound sleep is accompanied by increased serotonin and dopamine levels in the brain. In neurons, AANAT1 functions to limit the quantity and consolidation of nighttime sleep, but in astrocytes AANAT1 constrains the amount of rebound sleep that flies take in response to sleep deprivation. These findings distinguish sleep-control functions of AANAT1 in neurons and astrocytes, and identify a critical role for astrocytes in the regulation of monoamine bioavailability and calibration of the response to sleep need.\n\nHighlightsO_LIThe monoamine catabolic enzyme arylalkylamine N-acetyltransferase 1 (AANAT1) is expressed by astrocytes and subsets of serotonergic, glutamatergic, GABAergic and cholinergic neurons in the adult brain of Drosophila.\nC_LIO_LIAANAT1 limits accumulation of serotonin and dopamine in the brain upon sleep deprivation.\nC_LIO_LILoss of AANAT1 from astrocytes, but not from neurons, causes flies to increase their daytime rebound sleep in response to overnight sleep deprivation.\nC_LI

neuroscience↗