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12. Amyloid-beta Induces Sleep Fragmentation that is Rescued by Fatty Acid Binding Proteins in Drosophila

Author

Gerstner, Jason R., Lenz, Olivia, Vanderheyden, William M., Chan, May T., Pfeiffenberger, Cory, and Pack, Allan I.

Subjects
Sleep Wake Disorders, Amyloid beta-Peptides, fungi, Fatty Acid-Binding Proteins, Article, Animals, Genetically Modified, Disease Models, Animal, Mifepristone, Hormone Antagonists, Gene Expression Regulation, Animals, Drosophila Proteins, Humans, Drosophila, RNA, Messenger, Wakefulness, Sleep, Locomotion, Transcription Factors
Abstract

Disruption of sleep/wake activity in Alzheimer's disease (AD) patients significantly affects their quality of life and that of their caretakers and is a major contributing factor for institutionalization. Levels of amyloid-β (Aβ) have been shown to be regulated by neuronal activity and to correlate with the sleep/wake cycle. Whether consolidated sleep can be disrupted by Aβ alone is not well understood. We hypothesize that Aβ42 can increase wakefulness and disrupt consolidated sleep. Here we report that flies expressing the human Aβ42 transgene in neurons have significantly reduced consolidated sleep compared with control flies. Fatty acid binding proteins (Fabp) are small hydrophobic ligand carriers that have been clinically implicated in AD. Aβ42 flies that carry a transgene of either the Drosophila Fabp or the mammalian brain-type Fabp show a significant increase in nighttime sleep and long consolidated sleep bouts, rescuing the Aβ42-induced sleep disruption. These studies suggest that alterations in Fabp levels and/or activity may be associated with sleep disturbances in AD. Future work to determine the molecular mechanisms that contribute to Fabp-mediated rescue of Aβ42-induced sleep loss will be important for the development of therapeutics in the treatment of AD. © 2016 Wiley Periodicals, Inc.

Published
2016

13. Normal sleep requires the astrocyte brain-type fatty acid binding protein FABP7

Author

Gerstner, Jason R., primary, Perron, Isaac J., additional, Riedy, Samantha M., additional, Yoshikawa, Takeo, additional, Kadotani, Hiroshi, additional, Owada, Yuji, additional, Van Dongen, Hans P. A., additional, Galante, Raymond J., additional, Dickinson, Kaitlin, additional, Yin, Jerry C. P., additional, Pack, Allan I., additional, and Frank, Marcos G., additional

Published
2017
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16. Cycling Behavior and Memory Formation

Author

Gerstner, Jason R., Lyons, Lisa C., Wright, Kenneth P., Loh, Dawn H., Rawashdeh, Oliver, Eckel-Mahan, Kristin L., and Roman, Gregg W.

Subjects
Cognition, Biological Clocks, Memory, Animals, Association Learning, Humans, Sleep, Article, Phylogeny, Circadian Rhythm
Abstract

Circadian research has spent considerable effort in the determining clock output pathways, including identifying both physiological and behavioral processes that demonstrate significant time-of-day variation. Memory formation and consolidation represent notable processes shaped by endogenous circadian oscillators. To date, very few studies on memory mechanisms have considered potential confounding effects of time-of-day and the organism's innate activity cycles (e.g., nocturnal, diurnal, or crepuscular). The following studies highlight recent work describing this interactive role of circadian rhythms and memory formation, and were presented at a mini-symposium at the 2009 annual meeting of the Society for Neuroscience. The studies illustrate these time-of-day observations in a variety of behavioral paradigms and model organisms, including olfactory avoidance conditioning in Drosophila, long-term sensitization in Aplysia, active-avoidance conditioning in Zebrafish, and classical fear conditioning in rodents, suggesting that the circadian influence on memory behavior is highly conserved across species. Evidence also exists for a conserved mechanistic relationship between specific cycling molecules and memory formation, and the extent to which proper circadian cycling of these molecules is necessary for optimal cognitive performance. Studies describe the involvement of the core clock gene period, as well as vasoactive intestinal peptide, melatonin, and the cAMP/MAPK (cAMP/mitogen-activated protein kinase) cascade. Finally, studies in humans describe evidence for alterations in cognitive performance based on an interaction between sleep-wake homeostasis and the internal circadian clock. Conservation of a functional relationship between circadian rhythms with learning and memory formation across species provides a critical framework for future analysis of molecular mechanisms underlying complex behavior.

Published
2009

19. dCREB2-Mediated Enhancement of Memory Formation

Author

Tubon, Thomas C., primary, Zhang, Jiabin, additional, Friedman, Eugenia L., additional, Jin, Haining, additional, Gonzales, Erin D., additional, Zhou, Hong, additional, Drier, Diana, additional, Gerstner, Jason R., additional, Paulson, Emily A., additional, Fropf, Robin, additional, and Yin, Jerry C. P., additional

Published
2013
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29. ERK Phosphorylation Regulates Sleep and Plasticity in Drosophila.

Author

Vanderheyden, William M., Gerstner, Jason R., Tanenhaus, Anne, Yin, Jerry C., and Shaw, Paul J.

Subjects
*EXTRACELLULAR signal-regulated kinases, *SLEEP deprivation, *DROSOPHILA, *MATERIAL plasticity, *MITOGEN-activated protein kinases, *PHOSPHORYLATION, *TRANSGENIC insects, *FLIES
Abstract

Given the relationship between sleep and plasticity, we examined the role of Extracellular signal-regulated kinase (ERK) in regulating baseline sleep, and modulating the response to waking experience. Both sleep deprivation and social enrichment increase ERK phosphorylation in wild-type flies. The effects of both sleep deprivation and social enrichment on structural plasticity in the LNvs can be recapitulated by expressing an active version of ERK (UAS-ERKSEM) pan-neuronally in the adult fly using GeneSwitch (Gsw) Gsw-elav-GAL4. Conversely, disrupting ERK reduces sleep and prevents both the behavioral and structural plasticity normally induced by social enrichment. Finally, using transgenic flies carrying a cAMP response Element (CRE)-luciferase reporter we show that activating ERK enhances CRE-Luc activity while disrupting ERK reduces it. These data suggest that ERK phosphorylation is an important mediator in transducing waking experience into sleep. [ABSTRACT FROM AUTHOR]

Published
2013
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30. ERK Phosphorylation Regulates Sleep and Plasticity in Drosophila.

Author

Vanderheyden, William M., Gerstner, Jason R., Tanenhaus, Anne, Yin, Jerry C., and Shaw, Paul J.

Subjects
EXTRACELLULAR signal-regulated kinases, SLEEP deprivation, DROSOPHILA, MATERIAL plasticity, MITOGEN-activated protein kinases, PHOSPHORYLATION, TRANSGENIC insects, FLIES
Abstract

Given the relationship between sleep and plasticity, we examined the role of Extracellular signal-regulated kinase (ERK) in regulating baseline sleep, and modulating the response to waking experience. Both sleep deprivation and social enrichment increase ERK phosphorylation in wild-type flies. The effects of both sleep deprivation and social enrichment on structural plasticity in the LNvs can be recapitulated by expressing an active version of ERK (UAS-ERKSEM) pan-neuronally in the adult fly using GeneSwitch (Gsw) Gsw-elav-GAL4. Conversely, disrupting ERK reduces sleep and prevents both the behavioral and structural plasticity normally induced by social enrichment. Finally, using transgenic flies carrying a cAMP response Element (CRE)-luciferase reporter we show that activating ERK enhances CRE-Luc activity while disrupting ERK reduces it. These data suggest that ERK phosphorylation is an important mediator in transducing waking experience into sleep. [ABSTRACT FROM AUTHOR]

Published
2013
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31. Sleep pressure regulates mushroom body neural-glial interactions in Drosophila.

Author

Vanderheyden WM, Van Dongen HPA, Frank MG, and Gerstner JR

Abstract

Sleep is a behavior that exists broadly across animal phyla, from flies to humans, and is necessary for normal brain function. Recent studies in both vertebrates and invertebrates have suggested a role for glial cells in sleep regulatory processes. Changes in neural-glial interactions have been shown to be critical for synaptic plasticity and circuit function. Here, we wanted to test the hypothesis that changes in sleep pressure alters neural-glial interactions. In the fruit fly, Drosophila melanogaster , sleep is known to be regulated by mushroom body (MB) circuits. We used the technique GFP Reconstitution Across Synaptic Partners (GRASP) to test whether changes in sleep pressure affect neural-glial interactions between MB neurons and astrocytes, a specialized glial cell type known to regulate sleep in flies and mammals. The MB-astrocyte GRASP signal was reduced after 24 h of sleep deprivation, whereas the signal returned to baseline levels following 72 h of recovery. Social enrichment, which increases sleep drive, similarly reduced the MB-astrocyte GRASP signal. We did not observe any changes in the MB-astrocyte GRASP signal over time-of-day, or following paraquat exposure or starvation. These data suggest that changes in sleep pressure are linked to dynamic changes in neural-glial interactions between astrocytes and neuronal sleep circuits, which are not caused by normal rest-activity cycles or stressors.

Published
2019
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