Topical Collection "Neurotoxicity: Mechanisms and Potential Therapeutic Strategies"

A topical collection in Biomedicines (ISSN 2227-9059). This collection belongs to the section "Neurologic Diseases".

Editor

Prof. Dr. David R. Wallace
Website SciProfiles
Collection Editor
Department of Pharmacology and Toxicology, School of Biomedical Science, Oklahoma State University Center for Health Sciences, Tulsa, OK 74107, USA
Interests: environmental toxicology; heavy metals; pesticides; neural development; glioblastoma; neural degeneration; oxidative stress; apoptotic pathways; mitochondrial toxicity; energy utilization; mitochondrial DNA; mercury; cadmium; nickel; arsenic; organophosphate; organochlorine; pancreatic cancer; neuroblastoma; neuroglioma; dopamine uptake; toxicology of mixtures; blood-brain barrier transport mechanisms
Special Issues and Collections in MDPI journals

Topical Collection Information

Dear Colleagues,

We are constantly subjected to toxic insults, most of these insults going unnoticed. Whether it is the environment, occupational or intentional exposure, toxicants are a part of our daily lives. As we go through the day, exposure to toxic metals, chemical by-products, particulate matter, volatile gases, pesticides, etc., occurs constantly. In most instances, this exposure is at a very low level, but continues for an extended time. With chronic exposure, we slowly build deficits, such as a loss of free radical scavenging enzymes, altered protein production and epigenetic changes. Collectively leading to signs and symptoms of neurotoxicity. The intent of this Topical Collection is the discuss mechanisms leading to neurotoxicity, and from these mechanisms, what potential therapeutic strategies are being developed. We would like to bring together a diverse group who are examining many different perspectives of neurotoxicity along with groups developing therapeutics to alleviate or prevent these toxic insults.

Prof. David R Wallace
Collection Editor

Manuscript Submission Information

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Keywords

  • Astrocytes
  • Microglia
  • Neuroinflammation
  • Neurodegeneration
  • Oxidative Stress
  • protein degeneration
  • heavy metals
  • pesticides

Published Papers (1 paper)

2019

Open AccessArticle
Comprehensive Analysis of Neurotoxin-Induced Ablation of Dopaminergic Neurons in Zebrafish Larvae
Biomedicines 2020, 8(1), 1; https://doi.org/10.3390/biomedicines8010001 - 28 Dec 2019
Cited by 1
Abstract
Neurotoxin exposure of zebrafish larvae has been used to mimic a Parkinson’s disease (PD) phenotype and to facilitate high-throughput drug screening. However, the vulnerability of zebrafish to various neurotoxins was shown to be variable. Here, we provide a direct comparison of ablative effectiveness [...] Read more.
Neurotoxin exposure of zebrafish larvae has been used to mimic a Parkinson’s disease (PD) phenotype and to facilitate high-throughput drug screening. However, the vulnerability of zebrafish to various neurotoxins was shown to be variable. Here, we provide a direct comparison of ablative effectiveness in order to identify the optimal neurotoxin-mediated dopaminergic (DAnergic) neuronal death in larval zebrafish. Transgenic zebrafish, Tg(dat:eGFP), were exposed to different concentrations of the neurotoxins MPTP, MPP+, paraquat, 6-OHDA, and rotenone for four days, starting at three days post-fertilization. The LC50 of each respective neurotoxin concentration was determined. Confocal live imaging on Tg(dat:eGFP) showed that MPTP, MPP+, and rotenone caused comparable DAnergic cell loss in the ventral diencephalon (vDC) region while, paraquat and 6-OHDA caused fewer losses of DAnergic cells. These results were further supported by respective gene expression analyses of dat, th, and p53. Importantly, the loss of DAnergic cells from exposure to MPTP, MPP+, and rotenone impacted larval locomotor function. MPTP induced the largest motor deficit, but this was accompanied by the most severe morphological impairment. We conclude that, of the tested neurotoxins, MPP+ recapitulates a substantial degree of DAnergic ablation and slight locomotor perturbations without systemic defects indicative of a Parkinsonian phenotype. Full article
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Figure 1

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