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NEUROPROTECTION AGAINST OXIDATIVE STRESS USING RESVERATROL-INSPIRED ANALOGS
Title
NEUROPROTECTION AGAINST OXIDATIVE STRESS USING RESVERATROL-INSPIRED ANALOGS.
Creator
Simonson, Alec Jordan, Dawson-Scully, Ken, Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
Abstract/Description
Synaptic transmission is a mechanism that makes life possible for many organisms. Damaging this crucial process, such as with a buildup of Reactive Oxygen Species (ROS), is extremely detrimental for the entire organism. Previously, the Dawson-Scully lab has determined that exposure of the Drosophila melanogaster neuromuscular junction (NMJ) to ROS accumulation can result in synaptic failure at a faster rate than saline controls (Caplan et al., 2013). To combat such effects, novel three...
Show moreSynaptic transmission is a mechanism that makes life possible for many organisms. Damaging this crucial process, such as with a buildup of Reactive Oxygen Species (ROS), is extremely detrimental for the entire organism. Previously, the Dawson-Scully lab has determined that exposure of the Drosophila melanogaster neuromuscular junction (NMJ) to ROS accumulation can result in synaptic failure at a faster rate than saline controls (Caplan et al., 2013). To combat such effects, novel three-dimensional Resveramorph compounds were created to act as a neuroprotective agent against the harmful effects of acute oxidative stress (Bollinger et al., 2019; Sial et al., 2019). With the initial Resveramorph compounds demonstrating neuroprotective effects, additional analysis of other Resveramorph compounds were of interest to better understand their role in neuroprotection. Further testing of these compounds allows for the investigation of how chemical structure affects a compound’s neuroprotective activity.
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Date Issued
2021
PURL
http://purl.flvc.org/fau/fd/FA00013687
Subject Headings
Resveratrol, Neuroprotective agents
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)
USING ELECTROSHOCK TO PROBE MECHANISMS OF HERBICIDE NEUROTOXICITY AND NOVEL NEUROPROTECTIVE COMPOUNDS IN CAENORHABDITIS ELEGANS AND DROSOPHILA MELANOGASTER
Title
USING ELECTROSHOCK TO PROBE MECHANISMS OF HERBICIDE NEUROTOXICITY AND NOVEL NEUROPROTECTIVE COMPOUNDS IN CAENORHABDITIS ELEGANS AND DROSOPHILA MELANOGASTER.
Creator
Naraine, Akshay S., Dawson-Scully, Kenneth, Milton, Sarah, Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
Abstract/Description
The communication in the nervous system is a pharmacological balance between excitatory and inhibitory signals, and seizure behavior is one of the most common manifestations of when an imbalance occurs. Environmental toxins can cause significant disruption of excitation-inhibition balance, but while some toxins, like nerve agents, have known targets and require novel antidotes, some have unknown neurobiological mechanisms and require exploration. Of particular concern, there is little...
Show moreThe communication in the nervous system is a pharmacological balance between excitatory and inhibitory signals, and seizure behavior is one of the most common manifestations of when an imbalance occurs. Environmental toxins can cause significant disruption of excitation-inhibition balance, but while some toxins, like nerve agents, have known targets and require novel antidotes, some have unknown neurobiological mechanisms and require exploration. Of particular concern, there is little knowledge on how herbicides may affect neurological signaling. Glyphosate, the world’s most popular herbicide, was found to be in 80% of people’s urine, and since it is so prevalent, it is critical to understand its impact on both excitatory and inhibitory signaling. We used an electroshock assay developed for C. elegans to uncover evidence that glyphosate, and the commercial formula Roundup, disrupted the excitation-inhibition balance by blocking GABA-A receptors. This presented a novel hypothesis of an inhibitory neurobiological target for glyphosate. As glutamate is the major excitatory neurotransmitter in the human central nervous system, an electrophysiology assay using Drosophila was used and found that Roundup, but not glyphosate, reduced synaptic viability. This result directs attention to the undisclosed adjuvant component which may have a significant effect on synaptic transmission, though the exact mechanism requires further investigation.
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Date Issued
2023
PURL
http://purl.flvc.org/fau/fd/FA00014151
Subject Headings
Seizures, Neurotoxins, Neuroprotective agents, Herbicides--Toxicology
Format
Document (PDF)
Role of taurine in the central nervous system
Title
Role of taurine in the central nervous system.
Creator
Wu, Jang-Yen, Prentice, Howard
Date Issued
2010-08-24
PURL
http://purl.flvc.org/fau/fd/FADT3327262
Subject Headings
Central Nervous System --metabolism, Glutamic Acid --metabolism, Homeostasis --physiology, Neuroprotective Agents --metabolism, Neurotransmitter Agents --metabolism, Proto-Oncogene Proteins c-bcl-2 --metabolism, Receptors, Neurotransmitter --metabolism, Signal Transduction --physiology, Taurine, Taurine --metabolism, Neuroprotective Agents, Neurotransmitter Agents
Format
Document (PDF)
Protecting Synaptic Function From Acute Oxidative Stress: A Novel Role For Big K+ (BK) Channels And Resveratrol-Like Compounds
Title
Protecting Synaptic Function From Acute Oxidative Stress: A Novel Role For Big K+ (BK) Channels And Resveratrol-Like Compounds.
Creator
Bollinger, Wesley L., Dawson-Scully, Ken, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description
Oxidative stress causes neural damage and inhibits essential cellular processes, such as synaptic transmission. Despite this knowledge, currently available pharmaceutical agents cannot effectively protect neural cells from acute oxidative stress elicited by strokes, heart attacks, and traumatic brain injuries in a real life clinical setting. Our lab has developed an electrophysiology protocol to identify novel drugs that protect an essential cellular process (neurotransmission) from acute...
Show moreOxidative stress causes neural damage and inhibits essential cellular processes, such as synaptic transmission. Despite this knowledge, currently available pharmaceutical agents cannot effectively protect neural cells from acute oxidative stress elicited by strokes, heart attacks, and traumatic brain injuries in a real life clinical setting. Our lab has developed an electrophysiology protocol to identify novel drugs that protect an essential cellular process (neurotransmission) from acute oxidative stress-induced damage. Through this doctoral dissertation, we have identified three new drugs, including a Big K+ (BK) K+ channel blocker (iberiotoxin), resveratrol, and a custom made resveratrol-like compound (fly2) that protect synaptic function from oxidative stress-induced insults. Further developing these drugs as neuroprotective agents may prove transformative in protecting the human brain from acute oxidative stress elicited by strokes, heart attacks, and traumatic brain injuries. Inhibiting the protein kinase G (PKG) pathway protects neurotransmission from acute oxidative stress. This dissertation has expanded upon these findings by determining that the PKG pathway and BK K+ channels function through independent biochemical pathways to protect neurotransmission from acute oxidative stress. Taken together, this dissertation has identified two classes of compounds that protect neurotransmission from acute oxidative stress, including resveratrol-like compounds (resveratrol, fly2) and a BK K+ channel inhibitor (iberiotoxin). Further developing these drugs in clinical trials may finally lead to the development of an effective neuroprotective agent.
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Date Issued
2018
PURL
http://purl.flvc.org/fau/fd/FA00013054
Subject Headings
Neural transmission., Oxidative stress., Large-Conductance Calcium-Activated Potassium Channels., Neuroprotective Agents.
Format
Document (PDF)
Neuroprotection from induced glutamate excitotoxicity by Conus brunneus conopeptides in a stroke-related model
Title
Neuroprotection from induced glutamate excitotoxicity by Conus brunneus conopeptides in a stroke-related model.
Creator
Crouch, Rebecca A., Charles E. Schmidt College of Science, Department of Chemistry and Biochemistry
Abstract/Description
Cone snails are carnivorous marine mollusks, utilizing their neuropeptide-rich venom for prey capture. The venom of Conus brunneus, a wide-spread Eastern Pacific vermivore, has not been extensively studied. In the current work, peptides from the dissected venom were characterized and tested using preliminary bioassays. Six peptides (A-F) were isolated and tested. Three peptide identities were determined by comparison with previously reported data: bru9a (A), bru3a (F), and an a-conotoxin (E)....
Show moreCone snails are carnivorous marine mollusks, utilizing their neuropeptide-rich venom for prey capture. The venom of Conus brunneus, a wide-spread Eastern Pacific vermivore, has not been extensively studied. In the current work, peptides from the dissected venom were characterized and tested using preliminary bioassays. Six peptides (A-F) were isolated and tested. Three peptide identities were determined by comparison with previously reported data: bru9a (A), bru3a (F), and an a-conotoxin (E). Preliminary screening in a stroke-related model of induced glutamate excitotoxicity in primary neuronal cells and PC12 cell cultures indicated potential neuroprotective activity of peptide fractions A, D, and F. Further testing is necessary to determine and verify structure, activity, target, and mechanism of action of the promising peptides from C. brunneus, which may prove effective neuropharmacological agents to treat stroke.
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Date Issued
2013
PURL
http://purl.flvc.org/fcla/dt/3362331
Subject Headings
Gastropoda, Venom, Therapeutic use, Peptides, Structure, Neuroprotective agents, Central nervous system, Diseases, Treatment
Format
Document (PDF)