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The characterization of both glial and neuronal mechanisms in the modulation of neuroprotection via the PKG pathway
Title
The characterization of both glial and neuronal mechanisms in the modulation of neuroprotection via the PKG pathway.
Creator
Krill, Jennifer L., Dawson-Scully, Ken, Graduate College
Abstract/Description
Previous work demonstrates that PKG pathway modulation in Drosophila controls tolerance to stress in adults and larvae. Through the use of genetics and pharmacology, PKG inhibition leads to significant protection of function while activation causes increased sensitivity and early coma onset. In this study we investigate the effect of PKG modulation on neurons and glia during acute hyperthermia, and begin to determine the underlying physiological contributions of both tissues. Glia have been...
Show morePrevious work demonstrates that PKG pathway modulation in Drosophila controls tolerance to stress in adults and larvae. Through the use of genetics and pharmacology, PKG inhibition leads to significant protection of function while activation causes increased sensitivity and early coma onset. In this study we investigate the effect of PKG modulation on neurons and glia during acute hyperthermia, and begin to determine the underlying physiological contributions of both tissues. Glia have been found to influence single neuron activity and global brain function. Neurons, the most energy-demanding cells in our bodies, are most sensitive to stress. As humans, our neurons function under stress until permanent failure, resulting in brain damage and even death. Insects are much more tolerant to environmental stressors. Although stress-activated protective pathways are highly conserved in both insects and humans, their outcome on neuronal function and survival are very different.
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Date Issued
2014
PURL
http://purl.flvc.org/fau/fd/FA00005829
Format
Document (PDF)
Effects of cGMP-dependent protein kinase signaling in Drosophila S2 cells subjected to anoxia and oxidative stress
Title
Effects of cGMP-dependent protein kinase signaling in Drosophila S2 cells subjected to anoxia and oxidative stress.
Creator
Makhnyeva, Olena, Milton, Sarah L., Dawson-Scully, Ken, Graduate College
Abstract/Description
Ischemic stroke is one of the leading causes of human death worldwide. It occurs due to high susceptibility of neurons to anoxia and reoxygenation. Unlike mammals, invertebrate Drosophila melanogaster withstands low oxygen levels without showing pathology. In the present study, Drosophila Schneider (S2) cells were employed to investigate the role of the cGMP-dependent Protein Kinase (PKG) signaling pathway in Drosophila anoxia-tolerance in vitro. This was accomplished by subjecting cells to...
Show moreIschemic stroke is one of the leading causes of human death worldwide. It occurs due to high susceptibility of neurons to anoxia and reoxygenation. Unlike mammals, invertebrate Drosophila melanogaster withstands low oxygen levels without showing pathology. In the present study, Drosophila Schneider (S2) cells were employed to investigate the role of the cGMP-dependent Protein Kinase (PKG) signaling pathway in Drosophila anoxia-tolerance in vitro. This was accomplished by subjecting cells to chemical anoxia and oxidative stress concurrently with treatments by pharmacological agents affecting specific targets of the PKG pathway and assessing cytotoxicity. In this study, activation of the PKG pathway protected S2 cells from the aforementioned stresses. The results of this study may lead to a better understanding of fruit fly’s innate anoxia-tolerance strategies. Consequently, this knowledge may be used to identify potential therapeutic targets to prevent detrimental neurological effects of an ischemic stroke in humans.
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Date Issued
2014
PURL
http://purl.flvc.org/fau/fd/FA00005837
Format
Document (PDF)
Core clock genes modulate the sleep-feeding axis
Title
Core clock genes modulate the sleep-feeding axis.
Creator
Murphy, Keith Richard, Bruce, Kimberly, Dawson-Scully, Ken, Graduate College, Ja, William W.
Abstract/Description
Sleep and feeding are processes essential to nearly all complex organisms, impacting the behavioral output of an animal through homeostatic drive. In Drosophila melanogaster it has been shown that starvation leads to sleep suppression through the signaling of core clock proteins that regulate the animal circadian rhythm. Furthermore overexpression of short neuropeptide, a sleep-promoting inhibitory modulator, increases sleep in animals and alters feeding behavior. While these findings provide...
Show moreSleep and feeding are processes essential to nearly all complex organisms, impacting the behavioral output of an animal through homeostatic drive. In Drosophila melanogaster it has been shown that starvation leads to sleep suppression through the signaling of core clock proteins that regulate the animal circadian rhythm. Furthermore overexpression of short neuropeptide, a sleep-promoting inhibitory modulator, increases sleep in animals and alters feeding behavior. While these findings provide a framework of the interaction between the pressures to feed and sleep, they are bi-modal shifts, limiting the understanding of this relationship between to its extreme states. Using the Activity Recording CAFÉ ARC, a tool for measuring the sleep and feeding of individual flies, we tuned either behavior and observed corresponding effects. By shifting food concentrations we are able to control hunger state of an animal while recording its sleep and activity patterns. By coupling this system with a gentle air puff we were also able to control sleep while measuring feeding. We found that the hunger state of an animal had a direct effect on sleep and sleep consolidation. Conversely, we show that increasing sleep pressure led to increased feeding and reduced satiety as calculated through the animal’s prandial behavior. In addition, we show that the direct relationship of the sleep/feeding is disrupted by core clock gene mutations but not by secondary clock genes such as period. By use of the ARC and bi-directional perturbation, we provide a higher resolution understanding of the sleep-feeding axis.
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Date Issued
2014
PURL
http://purl.flvc.org/fau/fd/FA00005843
Format
Document (PDF)
Sulindac enhances the killing of cancer cells exposed to oxidative stress
Title
Sulindac enhances the killing of cancer cells exposed to oxidative stress.
Creator
Kreymerman, Alexander, Ayyanathan, Kasirajan, Kesaraju, Shailaja, Dawson-Scully, Ken, Weissbach, Herbert, Graduate College
Date Issued
2011-04-08
PURL
http://purl.flvc.org/fcla/dt/3164545
Subject Headings
Nonsteroidal anti-inflammatory agents, Oxidative stress, Mitochondrial pathology
Format
Document (PDF)
Rapid neuroprotection from acute oxidative stress
Title
Rapid neuroprotection from acute oxidative stress.
Creator
Caplan, Stacee Lee, Dawson-Scully, Ken, Milton, Sarah L., Graduate College
Date Issued
2011-04-08
PURL
http://purl.flvc.org/fcla/dt/3164512
Subject Headings
Stress --physiology, Protein kinases, Neuroprotective agents
Format
Document (PDF)