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Neurotoxins in the Neurosciences: Molecular Mechanisms and Applications
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Neurotoxins in the Neurosciences: Molecular Mechanisms and Applications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 November 2019) | Viewed by 26599

Special Issue Editors

Prof. Dr. Andreas Wree

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Guest Editor
Institute of Anatomy, Rostock University Medical Center, Gertrudenstrasse 9, 18057 Rostock, Germany
Interests: botulinum-neurotoxin; receptors; imaging; animal models of neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Björn Spittau

E-Mail
Guest Editor
Department of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany
Interests: microglia; neuroinflammation; MPTP; animal models of neurodegenerative diseases

Special Issue Information

Dear Colleagues,

Neurotoxins are substances with very diverse chemical properties and functions, and act by very diverse mechanisms leading to either the disruption or destruction of distinct components within the nervous system, during development or in adulthood. Neurotoxins can be naturally derived or synthetic. Biological neurotoxins, which are effectively used by snakes, fungi and bacteria, differ in terms of the source, binding site and mechanisms of toxic action. According to their very special design and function, they are often used in experimental neuroscience, providing effective means by which certain elements of the nervous system can be accurately and efficiently targeted. As each toxin differs in action and binding site, this specificity can be used to study individual sites of the nervous system. For this reason, neurotoxins are considered excellent tools for understanding the complex nervous system.

In this Special Issue, we ask experts using biological and synthetic neurotoxins in experimental research to contribute manuscripts to increase the understanding of different aspects of neurotoxins.

Prof. Dr. Andreas Wree
Prof. Dr. Björn Spittau
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (5 papers)

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Research

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17 pages, 5857 KiB  
Article
New Engineered-Botulinum Toxins Inhibit the Release of Pain-Related Mediators
by Minhong Tang, Jianghui Meng and Jiafu Wang
Int. J. Mol. Sci. 2020, 21(1), 262; https://doi.org/10.3390/ijms21010262 - 30 Dec 2019
Cited by 15 | Viewed by 3289
Abstract
Targeted delivery of potent inhibitor of cytokine/pain-mediator into inflammatory or pain-sensing cells is a promising avenue for treating chronic pain, a world-wide major healthcare burden. An unmet need exists for a specific and effective delivery strategy. Herein, we describe a new approach using [...] Read more.
Targeted delivery of potent inhibitor of cytokine/pain-mediator into inflammatory or pain-sensing cells is a promising avenue for treating chronic pain, a world-wide major healthcare burden. An unmet need exists for a specific and effective delivery strategy. Herein, we describe a new approach using sortase to site-specifically ligate a non-toxic botulinum neurotoxin D (BoNT/D) core-therapeutic (synaptobrevin-cleaving protease and translocation domains) to cell-specific targeting ligands. An engineered core-therapeutic was efficiently ligated to IL-1β ligand within minutes. The resultant conjugate specifically entered into cultured murine primary macrophages, cleaved synaptobrevin 3 and inhibited LPS/IFN-γ evoked IL-6 release. Likewise, a CGRP receptor antagonist ligand delivered BoNT/D protease into sensory neurons and inhibited K+-evoked substance P release. As cytokines and neuropeptides are major regulators of inflammation and pain, blocking their release by novel engineered inhibitors highlights their therapeutic potential. Our report describes a new and widely-applicable strategy for the production of targeted bio-therapeutics for numerous chronic diseases. Full article
(This article belongs to the Special Issue Neurotoxins in the Neurosciences: Molecular Mechanisms and Applications)
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17 pages, 7447 KiB  
Article
MST1 Regulates Neuronal Cell Death via JNK/Casp3 Signaling Pathway in HFD Mouse Brain and HT22 Cells
by Mehtab Khan, Bart P. F. Rutten and Myeong Ok Kim
Int. J. Mol. Sci. 2019, 20(10), 2504; https://doi.org/10.3390/ijms20102504 - 21 May 2019
Cited by 31 | Viewed by 6015
Abstract
Oxidative stress has been considered as the main mediator in neurodegenerative diseases. A high-fat diet (HFD) and metabolic diseases result in oxidative stress generation, leading to various neurodegenerative diseases via molecular mechanisms that remain largely unknown. Protein kinases play an important role in [...] Read more.
Oxidative stress has been considered as the main mediator in neurodegenerative diseases. A high-fat diet (HFD) and metabolic diseases result in oxidative stress generation, leading to various neurodegenerative diseases via molecular mechanisms that remain largely unknown. Protein kinases play an important role in the homeostasis between cell survival and cell apoptosis. The mammalian sterile 20-like kinase-1 (MST1) protein kinase plays an important role in cellular apoptosis in different organ systems, including the central nervous system. In this study, we evaluated the MST1/c-Jun N-terminal kinase (JNK) dependent oxidative damage mediated cognitive dysfunction in HFD-fed mice and stress-induced hippocampal HT22 (mice hippocampal) cells. Our Western blot and immunofluorescence results indicate that HFD and stress-induced hippocampal HT22 cells activate MST1/JNK/Caspase-3 (Casp-3) signaling, which regulates neuronal cell apoptosis and beta-amyloid-cleaving enzyme (BACE1) expression and leads to impaired cognition. Moreover, MST1 expression inhibition by shRNA significantly reduced JNK/Casp-3 signaling. Our in vivo and in vitro experiments mimicking metabolic stress, such as a high-fat diet, hyperglycemia, and an inflammatory response, determined that MST1 plays a key regulatory role in neuronal cell death and cognition, suggesting that MST1 could be a potential therapeutic target for numerous neurodegenerative diseases. Full article
(This article belongs to the Special Issue Neurotoxins in the Neurosciences: Molecular Mechanisms and Applications)
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20 pages, 2609 KiB  
Article
Botulinum Neurotoxin-A Injected Intrastriatally into Hemiparkinsonian Rats Improves the Initiation Time for Left and Right Forelimbs in Both Forehand and Backhand Directions
by Veronica Antipova, Carsten Holzmann, Alexander Hawlitschka and Andreas Wree
Int. J. Mol. Sci. 2019, 20(4), 992; https://doi.org/10.3390/ijms20040992 - 25 Feb 2019
Cited by 7 | Viewed by 3050
Abstract
Forelimb stepping is a widely used test for the assessment of forelimb akinesia in hemiparkinsonian (hemi-PD) rats. The initiation time (IT) is considered the most sensitive parameter in the stepping test procedure. Here we propose a novel, reliable, and simple method for the [...] Read more.
Forelimb stepping is a widely used test for the assessment of forelimb akinesia in hemiparkinsonian (hemi-PD) rats. The initiation time (IT) is considered the most sensitive parameter in the stepping test procedure. Here we propose a novel, reliable, and simple method for the measurement of IT of both forelimbs in both forehand and backhand directions in rats. Evaluating the same videos taken for quantifying adjusting steps, IT measurements were done without additional experiments. This is in contrast to the classical approach introduced by Olsson et al. (1995), in which separate experiments are necessary. We successfully applied our approach to hemi-PD rats intrastriatally treated with botulinum neurotoxin-A (BoNT-A). In naïve rats, an IT of about 0.62 s was found, and in right-sided hemi-PD rats the IT of the left forepaw increased to about 3.62 s. These hemi-PD rats showed, however, reduced ITs of the impaired left forepaws 1 month and the second time 7 months after induction of hemi-PD via the injection of 1 ng BoNT-A into the ipsilateral striatum, depending on post BoNT-A survival time. The method described offers the possibility of a precise and animal-friendly evaluation of IT in rats, including the beneficial effect of BoNT-A treatment in hemi-PD rats. Full article
(This article belongs to the Special Issue Neurotoxins in the Neurosciences: Molecular Mechanisms and Applications)
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Review

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9 pages, 437 KiB  
Review
Application of the Scorpion Neurotoxin AaIT against Insect Pests
by Sheng-Qun Deng, Jia-Ting Chen, Wen-Wen Li, Min Chen and Hong-Juan Peng
Int. J. Mol. Sci. 2019, 20(14), 3467; https://doi.org/10.3390/ijms20143467 - 15 Jul 2019
Cited by 14 | Viewed by 4896
Abstract
Androctonus australis Hector insect toxin (AaIT), an insect-selective toxin, was identified in the venom of the scorpion Androctonus australis. The exclusive and specific target of the toxin is the voltage-gated sodium channels of the insect, resulting in fast excitatory paralysis and even [...] Read more.
Androctonus australis Hector insect toxin (AaIT), an insect-selective toxin, was identified in the venom of the scorpion Androctonus australis. The exclusive and specific target of the toxin is the voltage-gated sodium channels of the insect, resulting in fast excitatory paralysis and even death. Because of its strict toxic selectivity and high bioactivity, AaIT has been widely used in experiments exploring pest bio-control. Recombinant expression of AaIT in a baculovirus or a fungus can increase their virulence to insect pests and diseases vectors. Likewise, transgenic plants expressing AaIT have notable anti-insect activity. AaIT is an efficient toxin and has great potential to be used in the development of commercial insecticides. Full article
(This article belongs to the Special Issue Neurotoxins in the Neurosciences: Molecular Mechanisms and Applications)
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11 pages, 782 KiB  
Review
Arsenic Neurotoxicity in Humans
by Hitoshi Mochizuki
Int. J. Mol. Sci. 2019, 20(14), 3418; https://doi.org/10.3390/ijms20143418 - 11 Jul 2019
Cited by 124 | Viewed by 8820
Abstract
Arsenic (As) contamination affects hundreds of millions of people globally. Although the number of patients with chronic As exposure is large, the symptoms and long-term clinical courses of the patients remain unclear. In addition to reviewing the literature on As contamination and toxicity, [...] Read more.
Arsenic (As) contamination affects hundreds of millions of people globally. Although the number of patients with chronic As exposure is large, the symptoms and long-term clinical courses of the patients remain unclear. In addition to reviewing the literature on As contamination and toxicity, we provide useful clinical information on medical care for As-exposed patients. Further, As metabolite pathways, toxicity, speculated toxicity mechanisms, and clinical neurological symptoms are documented. Several mechanisms that seem to play key roles in As-induced neurotoxicity, including oxidative stress, apoptosis, thiamine deficiency, and decreased acetyl cholinesterase activity, are described. The observed neurotoxicity predominantly affects peripheral nerves in sensory fibers, with a lesser effect on motor fibers. A sural nerve biopsy showed the axonal degeneration of peripheral nerves mainly in small myelinated and unmyelinated fibers. Exposure to high concentrations of As causes severe central nervous system impairment in infants, but no or minimal impairment in adults. The exposure dose–response relationship was observed in various organs including neurological systems. The symptoms caused by heavy metal pollution (including As) are often nonspecific. Therefore, in order to recognize patients experiencing health problems caused by As, a multifaceted approach is needed, including not only clinicians, but also specialists from multiple fields. Full article
(This article belongs to the Special Issue Neurotoxins in the Neurosciences: Molecular Mechanisms and Applications)
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