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Special Issue "Neurotoxins: Health Threats and Biological Tools"

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A special issue of Toxins (ISSN 2072-6651).

Deadline for manuscript submissions: closed (31 January 2014)

Special Issue Editor

Guest Editor
Prof. Dr. Peter S. Spencer

Department of Neurology, School of Medicine, and Oregon Institute for Occupational Health Sciences, Oregon Health & Science University, Portland, OR 97239, USA
E-Mail
Phone: 503 209-0986
Interests: neurotoxinology (plant, fungal); neurotoxicology; systems biology; human disease Contribution: Special Issue: Neurotoxins: Health Threats and Biological Tools

Special Issue Information

Dear Colleagues,

Neurotoxicity is a direct or indirect effect of chemical substances that disrupt nervous system function. Substances with these properties—“neurotoxins”—include the products, secretions and contents of certain bacteria, endophyte and exophyte fungi, ancient and modern plants, coelenterates, insects, arachnids, molluscs, amphibia, reptilia, fish, and mammals. Hundreds of naturally occurring toxins with systemic neurotoxic potential in humans and animals are known, but rarely does human and veterinary medicine connect, let alone synergize. Many neurotoxins are used as experimental tools to explore cellular function and dysfunction. Neurotoxins may act at the level of DNA, coding and non-coding RNAs, protein, and other macromolecules. Some directly perturb neural function; others interfere with metabolic processes on which the nervous system is especially dependent, and amino acid neurotoxins might even be incorporated into brain proteins with unknown functional outcomes. The effects of neurotoxins find expression in nervous system dysfunction in the presence or absence visible structural damage. Perturbations may appear and disappear rapidly, or may evolve and regress over days, weeks, years, or even decades. This special issue seeks papers that illuminate the mechanisms of natural neurotoxins and those that bridge neurotoxin mechanisms with associated human and animal disease.

Prof. Dr. Peter Spencer
Guest Editor

Submission

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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on theInstructions for Authors page. Toxins is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

Keywords

  • chemical structure of naturally occurring neurotoxins
  • molecular mechanisms of neurotoxin action
  • gene/protein-neurotoxin interactions
  • neurotoxins as biological tools
  • neurotoxins linked human neurological disease
  • neurotoxins linked to veterinary neurology

Published Papers (5 papers)

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Research

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Open AccessArticle Microcystins Alter Chemotactic Behavior in Caenorhabditis elegans by Selectively Targeting the AWA Sensory Neuron
Toxins 2014, 6(6), 1813-1836; doi:10.3390/toxins6061813
Received: 28 January 2014 / Revised: 17 May 2014 / Accepted: 28 May 2014 / Published: 10 June 2014
Cited by 3 | PDF Full-text (1399 KB) | HTML Full-text | XML Full-text
Abstract
Harmful algal blooms expose humans and animals to microcystins (MCs) through contaminated drinking water. While hepatotoxicity following acute exposure to MCs is well documented, neurotoxicity after sub-lethal exposure is poorly understood. We developed a novel statistical approach using a generalized linear model and
[...] Read more.
Harmful algal blooms expose humans and animals to microcystins (MCs) through contaminated drinking water. While hepatotoxicity following acute exposure to MCs is well documented, neurotoxicity after sub-lethal exposure is poorly understood. We developed a novel statistical approach using a generalized linear model and the quasibinomial family to analyze neurotoxic effects in adult Caenorhabditis elegans exposed to MC-LR or MC-LF for 24 h. Selective effects of toxin exposure on AWA versus AWC sensory neuron function were determined using a chemotaxis assay. With a non-monotonic response MCs altered AWA but not AWC function, and MC-LF was more potent than MC-LR. To probe a potential role for protein phosphatases (PPs) in MC neurotoxicity, we evaluated the chemotactic response in worms exposed to the PP1 inhibitor tautomycin or the PP2A inhibitor okadaic acid for 24 h. Okadaic acid impaired both AWA and AWC function, while tautomycin had no effect on function of either neuronal cell type at the concentrations tested. These findings suggest that MCs alter the AWA neuron at concentrations that do not cause AWC toxicity via mechanisms other than PP inhibition. Full article
(This article belongs to the Special Issue Neurotoxins: Health Threats and Biological Tools)
Open AccessArticle Botulinum Neurotoxin A Complex Recognizes Host Carbohydrates through Its Hemagglutinin Component
Toxins 2014, 6(2), 624-635; doi:10.3390/toxins6020624
Received: 24 December 2013 / Revised: 15 January 2014 / Accepted: 5 February 2014 / Published: 12 February 2014
Cited by 8 | PDF Full-text (1775 KB) | HTML Full-text | XML Full-text
Abstract
Botulinum neurotoxins (BoNTs) are potent bacterial toxins. The high oral toxicity of BoNTs is largely attributed to the progenitor toxin complex (PTC), which is assembled from BoNT and nontoxic neurotoxin-associated proteins (NAPs) that are produced together with BoNT in bacteria. Here, we performed
[...] Read more.
Botulinum neurotoxins (BoNTs) are potent bacterial toxins. The high oral toxicity of BoNTs is largely attributed to the progenitor toxin complex (PTC), which is assembled from BoNT and nontoxic neurotoxin-associated proteins (NAPs) that are produced together with BoNT in bacteria. Here, we performed ex vivo studies to examine binding of the highly homogeneous recombinant NAPs to mouse small intestine. We also carried out the first comprehensive glycan array screening with the hemagglutinin (HA) component of NAPs. Our data confirmed that intestinal binding of the PTC is partly mediated by the HA moiety through multivalent interactions between HA and host carbohydrates. The specific HA-carbohydrate recognition could be inhibited by receptor-mimicking saccharides. Full article
(This article belongs to the Special Issue Neurotoxins: Health Threats and Biological Tools)

Review

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Open AccessReview Secreted Phospholipases A2 of Snake Venoms: Effects on the Peripheral Neuromuscular System with Comments on the Role of Phospholipases A2 in Disorders of the CNS and Their Uses in Industry
Toxins 2013, 5(12), 2533-2571; doi:10.3390/toxins5122533
Received: 8 October 2013 / Revised: 2 December 2013 / Accepted: 10 December 2013 / Published: 17 December 2013
Cited by 7 | PDF Full-text (10055 KB) | HTML Full-text | XML Full-text
Abstract
Neuro- and myotoxicological signs and symptoms are significant clinical features of envenoming snakebites in many parts of the world. The toxins primarily responsible for the neuro and myotoxicity fall into one of two categories—those that bind to and block the post-synaptic acetylcholine receptors
[...] Read more.
Neuro- and myotoxicological signs and symptoms are significant clinical features of envenoming snakebites in many parts of the world. The toxins primarily responsible for the neuro and myotoxicity fall into one of two categories—those that bind to and block the post-synaptic acetylcholine receptors (AChR) at the neuromuscular junction and neurotoxic phospholipases A2 (PLAs) that bind to and hydrolyse membrane phospholipids of the motor nerve terminal (and, in most cases, the plasma membrane of skeletal muscle) to cause degeneration of the nerve terminal and skeletal muscle. This review provides an introduction to the biochemical properties of secreted sPLA2s in the venoms of many dangerous snakes and a detailed discussion of their role in the initiation of the neurologically important consequences of snakebite. The rationale behind the experimental studies on the pharmacology and toxicology of the venoms and isolated PLAs in the venoms is discussed, with particular reference to the way these studies allow one to understand the biological basis of the clinical syndrome. The review also introduces the involvement of PLAs in inflammatory and degenerative disorders of the central nervous system (CNS) and their commercial use in the food industry. It concludes with an introduction to the problems associated with the use of antivenoms in the treatment of neuro-myotoxic snakebite and the search for alternative treatments. Full article
(This article belongs to the Special Issue Neurotoxins: Health Threats and Biological Tools)
Open AccessReview Sialorrhea: Anatomy, Pathophysiology and Treatment with Emphasis on the Role of Botulinum Toxins
Toxins 2013, 5(5), 1010-1031; doi:10.3390/toxins5051010
Received: 1 March 2013 / Revised: 9 April 2013 / Accepted: 24 April 2013 / Published: 21 May 2013
Cited by 22 | PDF Full-text (774 KB) | HTML Full-text | XML Full-text
Abstract
Sialorrhea or excessive drooling is a major issue in children with cerebral palsy and adults with neurodegenerative disorders. In this review, we describe the clinical features, anatomy and physiology of sialorrhea, as well as a review of the world literature on medical treatment
[...] Read more.
Sialorrhea or excessive drooling is a major issue in children with cerebral palsy and adults with neurodegenerative disorders. In this review, we describe the clinical features, anatomy and physiology of sialorrhea, as well as a review of the world literature on medical treatment using Yale University’s search engine; including but not limited to Medline and Erasmus. Level of drug efficacy is defined according to the guidelines of American Academy of Neurology. Current medical management is unsatisfactory. Topical agents (scopolamine and tropicamide) and oral agents (glyccopyrolate) combined render a level B evidence (probably effective); however, this treatment is associated with troublesome side effects. Double-blind and placebo-controlled studies of botulinum toxin (BoNT) provide a level A evidence for type B (two class I studies; effective and established) and both overall and individual B level of evidence for OnabotulinumtoxinA (A/Ona) and AbobotulinumtoxinA (A/Abo); these are probably effective. For IncobotulinumtoxinA (A/Inco), the level of evidence is U (insufficient) due to lack of blinded studies. Side effects are uncommon; transient and comparable between the two types of toxin. A clinical note at the end of this review comments on fine clinical points. Administration of BoNTs into salivary glands is currently the most effective way of treating sialorrhea. Full article
(This article belongs to the Special Issue Neurotoxins: Health Threats and Biological Tools)
Open AccessReview Hyperhidrosis: Anatomy, Pathophysiology and Treatment with Emphasis on the Role of Botulinum Toxins
Toxins 2013, 5(4), 821-840; doi:10.3390/toxins5040821
Received: 12 February 2013 / Revised: 27 March 2013 / Accepted: 12 April 2013 / Published: 23 April 2013
Cited by 32 | PDF Full-text (497 KB) | HTML Full-text | XML Full-text
Abstract
Clinical features, anatomy and physiology of hyperhidrosis are presented with a review of the world literature on treatment. Level of drug efficacy is defined according to the guidelines of the American Academy of Neurology. Topical agents (glycopyrrolate and methylsulfate) are evidence level B
[...] Read more.
Clinical features, anatomy and physiology of hyperhidrosis are presented with a review of the world literature on treatment. Level of drug efficacy is defined according to the guidelines of the American Academy of Neurology. Topical agents (glycopyrrolate and methylsulfate) are evidence level B (probably effective). Oral agents (oxybutynin and methantheline bromide) are also level B. In a total of 831 patients, 1 class I and 2 class II blinded studies showed level B efficacy of OnabotulinumtoxinA (A/Ona), while 1 class I and 1 class II study also demonstrated level B efficacy of AbobotulinumtoxinA (A/Abo) in axillary hyperhidrosis (AH), collectively depicting Level A evidence (established) for botulinumtoxinA (BoNT-A). In a comparator study, A/Ona and A/Inco toxins demonstrated comparable efficacy in AH. For IncobotulinumtoxinA (A/Inco) no placebo controlled studies exist; thus, efficacy is Level C (possibly effective) based solely on the aforementioned class II comparator study. For RimabotulinumtoxinB (B/Rima), one class III study has suggested Level U efficacy (insufficient data). In palmar hyperhidrosis (PH), there are 3 class II studies for A/Ona and 2 for A/Abo (individually and collectively level B for BoNT-A) and no blinded study for A/Inco (level U). For B/Rima the level of evidence is C (possibly effective) based on 1 class II study. Botulinum toxins (BoNT) provide a long lasting effect of 3–9 months after one injection session. Studies on BoNT-A iontophoresis are emerging (2 class II studies; level B); however, data on duration and frequency of application is inconsistent. Full article
(This article belongs to the Special Issue Neurotoxins: Health Threats and Biological Tools)

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