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Title: cGMP-Dependent Protein Kinase Inhibition Extends the Upper Temperature Limit of Stimulus-Evoked Calcium Responses in Motoneuronal Boutons of Drosophila melanogaster Larvae.
Creator: Krill, Jennifer L., Dawson-Scully, Ken, McCabe, Brian D.
Abstract/Description: While the mammalian brain functions within a very narrow range of oxygen concentrations and temperatures, the fruit fly, Drosophila melanogaster, has employed strategies to deal with a much wider range of acute environmental stressors. The foraging (for) gene encodes the cGMP-dependent protein kinase (PKG), has been shown to regulate thermotolerance in many stress-adapted species, including Drosophila, and could be a potential therapeutic target in the treatment of hyperthermia in mammals....
Show moreWhile the mammalian brain functions within a very narrow range of oxygen concentrations and temperatures, the fruit fly, Drosophila melanogaster, has employed strategies to deal with a much wider range of acute environmental stressors. The foraging (for) gene encodes the cGMP-dependent protein kinase (PKG), has been shown to regulate thermotolerance in many stress-adapted species, including Drosophila, and could be a potential therapeutic target in the treatment of hyperthermia in mammals. Whereas previous thermotolerance studies have looked at the effects of PKG variation on Drosophila behavior or excitatory postsynaptic potentials at the neuromuscular junction (NMJ), little is known about PKG effects on presynaptic mechanisms. In this study, we characterize presynaptic calcium ([Ca^2+]i) dynamics at the Drosophila larval NMJ to determine the effects of high temperature stress on synaptic transmission. We investigated the neuroprotective role of PKG modulation both genetically using RNA interference (RNAi), and pharmacologically, to determine if and how PKG affects presynaptic [Ca^2+]i dynamics during hyperthermia. We found that PKG activity modulates presynaptic neuronal Ca^2+ responses during acute hyperthermia, where PKG activation makes neurons more sensitive to temperatureinduced failure of Ca^2+ flux and PKG inhibition confers thermotolerance and maintains normal Ca^2+ dynamics under the same conditions. Targeted motoneuronal knockdown of PKG using RNAi demonstrated that decreased PKG expression was sufficient to confer thermoprotection. These results demonstrate that the PKG pathway regulates presynaptic motoneuronal Ca^2+ signaling to influence thermotolerance of presynaptic function during acute hyperthermia.
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Date Issued: 2016-10-06
PURL: http://purl.flvc.org/fau/fd/FAUIR000079
Format: Citation

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)

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)

Title: Influence of cGMP-dependent Protein Kinase Signaling Pathway in Time to Recovery from an Induced Electroconvulsive Seizure in D. melanogaster.
Creator: Leonor Miranda, Monica Risley, Ken Dawson-Scully
Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FAU_SR00000015
Subject Headings: College students --Research --United States.
Format: Document (PDF)

Title: Neuroprotection from Brain Anoxia and Reperfusion Injury During Stroke and Compositions of PKG Pathway Activators and Method of Use Thereof, 2011.
Creator: Dawson-Scully, Ken, Milton, Sara Louise, Florida Atlantic University
Abstract/Description: A pharmaceutical composition for treating or preventing one or both of neural anoxia and reperfusion injury, which includes a pharmacological activator of the PKG pathway, and methods of treating or preventing medical conditions using a pharmacological activator of the PKG pathway.
Date Issued: 2011
PURL: http://purl.flvc.org/fau/fd/FAUIR000258
Format: Document (PDF)

Title: Neuroprotection from Brain Anoxia and Reperfusion Injury During Stroke and Compositions of PKG Pathway Activators and Method of Use Thereof, 2012.
Creator: Dawson-Scully, Ken, Milton, Sara Louise, Florida Atlantic University
Abstract/Description: A pharmaceutical composition for treating or preventing one or both of neural anoxia and reperfusion injury, which includes a pharmacological activator of the PKG pathway, and methods of treating or preventing medical conditions using a pharmacological activator of the PKG pathway.
Date Issued: 2012
PURL: http://purl.flvc.org/fau/fd/FAUIR000257
Format: Document (PDF)

Title: Pushing the limit: Examining factors that affect anoxia tolerance in a single genotype of adult D. melanogaster.
Creator: Benasayag Meszaros, Raquel, Risley, Monica G., Hernandez, Priscilla, Fendrich, Margo, Dawson-Scully, Ken
Abstract/Description: Drosophila melanogaster is a promiscuous species that inhabits a large range of harsh environments including flooded habitats and varying temperature changes. To survive these environments, fruit flies have adapted mechanisms of tolerance that allow them to thrive. During exposure to anoxic stress, fruit flies and other poikilotherms enter into a reversible, protective coma. This coma can be manipulated based on controlled environmental conditions inside the laboratory. Here we utilize a...
Show moreDrosophila melanogaster is a promiscuous species that inhabits a large range of harsh environments including flooded habitats and varying temperature changes. To survive these environments, fruit flies have adapted mechanisms of tolerance that allow them to thrive. During exposure to anoxic stress, fruit flies and other poikilotherms enter into a reversible, protective coma. This coma can be manipulated based on controlled environmental conditions inside the laboratory. Here we utilize a common laboratory raised strain of D. melanogaster to characterize adaptation abilities to better understand coma recovery and survival limitations. Our goal is to mimic the fly’s natural environments (wet anoxia) and relate findings to a typical gas induced environment (dry anoxia) that is commonly used in a laboratory. Despite the abundance of research regarding acute and chronic anoxic exposure and cold stress, the literature is lacking evidence linking anoxic stress with variable environmental conditions such as animal age and stress duration. We present novel ways to assess coma recovery and survival using readily available laboratory tools. Our findings suggest that younger age, exposure to colder temperatures and wet environments increase resistance to anoxic stress.
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Date Issued: 2015-08-17
PURL: http://purl.flvc.org/fau/fd/FAUIR000065
Format: Citation

Title: A cGMP-dependent protein kinase (PKG) controls synaptic transmission tolerance to acute oxidative stress at the Drosophila larval neuromuscular junction.
Creator: Caplan, Stacee Lee, Milton, Sarah L., Dawson-Scully, Ken
Date Issued: 2013-02-01
PURL: http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1152_jn.00784.2011_1644861569
Format: Document (PDF)

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)

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)

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)

Title: Biological Benefit of the mCAT.
Creator: Frydman, Sylvia, Yousefzadeh, Matt, Niedernhofer, Laura, Dawson-Scully, Ken
Abstract/Description: Aging is associated with chronic diseases and is attributed to increased morbidity, mortality, and healthcare costs globally. Controversy exists over the root cause(s) of aging, nonetheless, extensive research links increased oxidants and reduced antioxidant buffering capacity with aging. The free radical theory of aging posits that the toxic build-up of free radicals and reactive oxygen species (ROS), promotes oxidative stress and enhances aging. Investigations involving the effect of...
Show moreAging is associated with chronic diseases and is attributed to increased morbidity, mortality, and healthcare costs globally. Controversy exists over the root cause(s) of aging, nonetheless, extensive research links increased oxidants and reduced antioxidant buffering capacity with aging. The free radical theory of aging posits that the toxic build-up of free radicals and reactive oxygen species (ROS), promotes oxidative stress and enhances aging. Investigations involving the effect of mitochondrial-targeted catalase, have proven to be beneficial in reducing ROS and increasing lifespan in naturally aged mice. My project involves investigating the biological benefit of the mCAT transgene and rescue of age-related functional decline in progeroid Ercc1-/∆ mice, an accelerated mouse model of aging. mCAT expression was shown to be largely restricted to the brain, heart, and muscle of mice. mCAT+/-;Ercc1-/∆ mice showed improvements in behavioral tests and health evaluations relative to controls.
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Date Issued: 2018
PURL: http://purl.flvc.org/fau/fd/FAU_SR00000036
Subject Headings: College students --Research --United States.
Format: Document (PDF)

Title: Compositions and Methods for Treating Neural Anoxia and Spreading Depression, 2009.
Creator: Dawson-Scully, Ken, Robertson, R. Meldrum, Florida Atlantic University, Armstrong, Gary A.B.
Abstract/Description: Compositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and...
Show moreCompositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and methods can be used to treat any condition associated with SD or anoxia, including stroke, spinal cord injury, neurogenerative disease, dizziness, headaches, and migraines.
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Date Issued: 2009
PURL: http://purl.flvc.org/fau/fd/FAUIR000255
Format: Document (PDF)

Title: Compositions and Methods for Treating Neural Anoxia and Spreading Depression, 2011.
Creator: Dawson-Scully, Ken, Robertson, R. Meldrum, Florida Atlantic University, Armstrong, Gary A.B.
Abstract/Description: Compositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and...
Show moreCompositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and methods can be used to treat any condition associated with SD or anoxia, including stroke, spinal cord injury, neurogenerative disease, dizziness, headaches, and migraines.
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Date Issued: 2011
PURL: http://purl.flvc.org/fau/fd/FAUIR000256
Format: Document (PDF)

Title: RanBP9 Plays a Critical Role in Neonatal Brain Development in Mice.
Creator: Palavicini, Juan Pablo, Lloyd, Brandon N., Hayes, Crystal D., Bianchi, Elisabetta, Kang, David E., Dawson-Scully, Ken, Lakshmana, Madepalli K., Okazawa, Hitoshi
Abstract/Description: RanBP9 is known to act as a scaffolding protein bringing together a variety of cell surface receptors and intracellular targets thereby regulating functions as diverse as neurite and axonal outgrowth, cell morphology, cell proliferation, myelination, gonad development, myofibrillogenesis and migration of neuronal precursors. Though RanBP9 is ubiquitously expressed in all tissues, brain is one of the organs with the highest expression levels of RanBP9. In the neurons, RanBP9 is localized...
Show moreRanBP9 is known to act as a scaffolding protein bringing together a variety of cell surface receptors and intracellular targets thereby regulating functions as diverse as neurite and axonal outgrowth, cell morphology, cell proliferation, myelination, gonad development, myofibrillogenesis and migration of neuronal precursors. Though RanBP9 is ubiquitously expressed in all tissues, brain is one of the organs with the highest expression levels of RanBP9. In the neurons, RanBP9 is localized mostly in the cytoplasm but also in the neurites and dendritic processes. We recently demonstrated that RanBP9 plays pathogenic role in Alzheimer’s disease. To understand the role of RanBP9 in the brain, here we generated RanBP9 null mice by genetrap based strategy. Most of Ran-/- mice die neonatally due to defects in the brain growth and development. The major defects include smaller cortical plate (CP), robustly enlarged lateral ventricles (LV) and reduced volume of hippocampus (HI). The lethal phenotype is due to a suckling defect as evidenced by lack of milk in the stomachs even several hours after parturition. The complex somatosensory system which is required for a behavior such as suckling appears to be compromised in Ran-/- mice due to under developed CP. Most importantly, RanBP9 phenotype is similar to ERK1/2 double knockout and the neural cell adhesion receptor, L1CAM knockout mice. Both ERK1 and L1CAM interact with RanBP9. Thus, RanBP9 appears to control brain growth and development through signaling mechanisms involving ERK1 and L1CAM receptor.
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Date Issued: 2013-06-26
PURL: http://purl.flvc.org/fau/fd/FAUIR000081
Format: Citation

Title: Glial Hsp70 Protects K+ Homeostasis in the Drosophila Brain during Repetitive Anoxic Depolarization.
Creator: Armstrong, Gary A. B., Xiao, Chengfeng, Krill, Jennifer L., Seroude, Laurent, Dawson-Scully, Ken, Robertson, R. Meldrum, Roman, Gregg
Abstract/Description: Neural tissue is particularly vulnerable to metabolic stress and loss of ion homeostasis. Repetitive stress generally leads to more permanent dysfunction but the mechanisms underlying this progression are poorly understood. We investigated the effects of energetic compromise in Drosophila by targeting the Na+/K+-ATPase. Acute ouabain treatment of intact flies resulted in subsequent repetitive comas that led to death and were associated with transient loss of K+ homeostasis in the brain. Heat...
Show moreNeural tissue is particularly vulnerable to metabolic stress and loss of ion homeostasis. Repetitive stress generally leads to more permanent dysfunction but the mechanisms underlying this progression are poorly understood. We investigated the effects of energetic compromise in Drosophila by targeting the Na+/K+-ATPase. Acute ouabain treatment of intact flies resulted in subsequent repetitive comas that led to death and were associated with transient loss of K+ homeostasis in the brain. Heat shock pre-conditioned flies were resistant to ouabain treatment. To control the timing of repeated loss of ion homeostasis we subjected flies to repetitive anoxia while recording extracellular [K+] in the brain. We show that targeted expression of the chaperone protein Hsp70 in glial cells delays a permanent loss of ion homeostasis associated with repetitive anoxic stress and suggest that this is a useful model for investigating molecular mechanisms of neuroprotection.
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Date Issued: 2011-12-12
PURL: http://purl.flvc.org/fau/fd/FAUIR000078
Format: Citation

Title: Pseudopterosin A: Protection of Synaptic Function and Potential as a Neuromodulatory Agent.
Creator: Caplan, Stacee Lee, Zheng, Bo, Dawson-Scully, Ken, White, Catherine, West, Lyndon
Date Issued: 2016-03-10
PURL: http://purl.flvc.org/fau/fd/FAUIR000130
Format: Citation

Title: Combination of Sulindac and Dichloroacetate Kills Cancer Cells via Oxidative Damage.
Creator: Ayyanathan, Kasirajan, Kesaraju, Shailaja, Dawson-Scully, Ken, Weissbach, Herbert, Bauer, Joseph Alan
Date Issued: 2012-07-17
PURL: http://purl.flvc.org/fau/fd/FAUIR000091
Format: Citation

Title: The HECT Family Ubiquitin Ligase EEL-1 Regulates Neuronal Function and Development.
Creator: Opperman, Karla J., Mulcahy, Ben, Giles, Andrew C., Risley, Monica G., Birnbaum, Rayna L., Tulgren, Erik D., Dawson-Scully, Ken, Zhen, Mei, Grill, Brock
Date Issued: 2017-04
PURL: http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1016_j.celrep.2017.04.003_1644939781
Format: Document (PDF)

Title: Modulating Behavior in C. elegans Using Electroshock and Antiepileptic Drugs.
Creator: Monica G. Risley, Stephanie P. Kelly, Kailiang Jia, Brock Grill, Ken Dawson- Scully
Abstract/Description: The microscopic nematode Caenorhabditis elegans has emerged as a valuable model for understanding the molecular and cellular basis of neurological disorders. The worm offers important physiological similarities to mammalian models such as conserved neuron morphology, ion channels, and neurotransmitters. While a wide-array of behavioral assays are available in C. elegans, an assay for electroshock/electroconvulsion remains absent. Here, we have developed a quantitative behavioral method to...
Show moreThe microscopic nematode Caenorhabditis elegans has emerged as a valuable model for understanding the molecular and cellular basis of neurological disorders. The worm offers important physiological similarities to mammalian models such as conserved neuron morphology, ion channels, and neurotransmitters. While a wide-array of behavioral assays are available in C. elegans, an assay for electroshock/electroconvulsion remains absent. Here, we have developed a quantitative behavioral method to assess the locomotor response following electric shock in C. elegans. Electric shock impairs normal locomotion, and induces paralysis and muscle twitching; after a brief recovery period, shocked animals resume normal locomotion. We tested electric shock responses in loss-of-function mutants for unc-25, which encodes the GABA biosynthetic enzyme GAD, and unc-49, which encodes the GABAA receptor. unc-25 and unc-49 mutants have decreased inhibitory GABAergic transmission to muscles, and take significantly more time to recover normal locomotion following electric shock compared to wild-type. Importantly, increased sensitivity of unc-25 and unc-49 mutants to electric shock is rescued by treatment with antiepileptic drugs, such as retigabine. Additionally, we show that pentylenetetrazol (PTZ), a GABAA receptor antagonist and proconvulsant in mammalian and C. elegans seizure models, increases susceptibility of worms to electric shock.
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FAUIR000530
Format: Document (PDF)

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