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USING ELECTROSHOCK TO PROBE MECHANISMS OF HERBICIDE NEUROTOXICITY AND NOVEL NEUROPROTECTIVE COMPOUNDS IN CAENORHABDITIS ELEGANS AND DROSOPHILA MELANOGASTER

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Date Issued:
2023
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 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.
Title: USING ELECTROSHOCK TO PROBE MECHANISMS OF HERBICIDE NEUROTOXICITY AND NOVEL NEUROPROTECTIVE COMPOUNDS IN CAENORHABDITIS ELEGANS AND DROSOPHILA MELANOGASTER.
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Name(s): Naraine, Akshay S. , author
Dawson-Scully, Kenneth, Thesis advisor
Milton, Sarah , Thesis advisor
Florida Atlantic University, Degree grantor
Department of Biological Sciences
Charles E. Schmidt College of Science
Type of Resource: text
Genre: Electronic Thesis Or Dissertation
Date Created: 2023
Date Issued: 2023
Publisher: Florida Atlantic University
Place of Publication: Boca Raton, Fla.
Physical Form: application/pdf
Extent: 155 p.
Language(s): English
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 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.
Identifier: FA00014151 (IID)
Degree granted: Dissertation (PhD)--Florida Atlantic University, 2023.
Collection: FAU Electronic Theses and Dissertations Collection
Note(s): Includes bibliography.
Subject(s): Seizures
Neurotoxins
Neuroprotective agents
Herbicides--Toxicology
Persistent Link to This Record: http://purl.flvc.org/fau/fd/FA00014151
Use and Reproduction: Copyright © is held by the author with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
Use and Reproduction: http://rightsstatements.org/vocab/InC/1.0/
Host Institution: FAU
Is Part of Series: Florida Atlantic University Digital Library Collections.