Neurotoxicity of the Cyanotoxin BMAA Through Axonal Degeneration and Intercellular Spreading.
Identifieur interne : 000742 ( Main/Exploration ); précédent : 000741; suivant : 000743Neurotoxicity of the Cyanotoxin BMAA Through Axonal Degeneration and Intercellular Spreading.
Auteurs : Vanessa X. Tan [Australie] ; Benjamin Lassus [France] ; Chai K. Lim [Australie] ; Philippe Tixador [France] ; Josquin Courte [France] ; Alban Bessede [France] ; Gilles J. Guillemin [Australie] ; Jean-Michel Peyrin [France]Source :
- Neurotoxicity research [ 1476-3524 ] ; 2017.
Abstract
β-Methylamino-L-alanine (BMAA) is implicated in neurodegeneration and neurotoxicity, particularly in ALS-Parkinson Dementia Complex. Neurotoxic properties of BMAA have been partly elucidated, while its transcellular spreading capacity has not been examined. Using reconstructed neuronal networks in microfluidic chips, separating neuronal cells into two subcompartments-(1) the proximal, containing first-order neuronal soma and dendrites, and (2) a distal compartment, containing either only axons originating from first-order neurons or second-order striatal neurons-creates a cortico-striatal network. Using this system, we investigated the toxicity and spreading of BMAA in murine primary neurons. We used a newly developed antibody to detect BMAA in cells. After treatment with 10 μM BMAA, the cyanotoxin was incorporated in first-degree neurons. We also observed a rapid trans-neuronal spread of BMAA to unexposed second-degree neurons in 48 h, followed by axonal degeneration, with limited somatic death. This in vitro study demonstrates BMAA axonal toxicity at sublethal concentrations and, for the first time, the transcellular spreading abilities of BMAA. This neuronal dying forward spread that could possibly be associated with progression of some neurodegenerative diseases especially amyotrophic lateral sclerosis.
DOI: 10.1007/s12640-017-9790-1
PubMed: 28842862
Affiliations:
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Tan</name><affiliation wicri:level="1"><nlm:affiliation>Macquarie University Centre for MND Research, Department of Biological Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Macquarie University Centre for MND Research, Department of Biological Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW</wicri:regionArea><wicri:noRegion>NSW</wicri:noRegion></affiliation></author><author><name sortKey="Lassus, Benjamin" sort="Lassus, Benjamin" uniqKey="Lassus B" first="Benjamin" last="Lassus">Benjamin Lassus</name><affiliation wicri:level="3"><nlm:affiliation>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Neuroscience Paris Seine, Adaptation Biologique et vieillissement, F-75005, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Neuroscience Paris Seine, Adaptation Biologique et vieillissement, F-75005, Paris</wicri:regionArea><placeName><settlement type="city">Paris</settlement><region type="région" nuts="2">Île-de-France</region></placeName></affiliation></author><author><name sortKey="Lim, Chai K" sort="Lim, Chai K" uniqKey="Lim C" first="Chai K" last="Lim">Chai K. 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Guillemin</name><affiliation wicri:level="1"><nlm:affiliation>Macquarie University Centre for MND Research, Department of Biological Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia. gilles.guillemin@mq.edu.au.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Macquarie University Centre for MND Research, Department of Biological Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW</wicri:regionArea><wicri:noRegion>NSW</wicri:noRegion></affiliation></author><author><name sortKey="Peyrin, Jean Michel" sort="Peyrin, Jean Michel" uniqKey="Peyrin J" first="Jean-Michel" last="Peyrin">Jean-Michel Peyrin</name><affiliation wicri:level="3"><nlm:affiliation>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Neuroscience Paris Seine, Adaptation Biologique et vieillissement, F-75005, Paris, France. jean-michel.peyrin@upmc.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Neuroscience Paris Seine, Adaptation Biologique et vieillissement, F-75005, Paris</wicri:regionArea><placeName><settlement type="city">Paris</settlement><region type="région" nuts="2">Île-de-France</region></placeName></affiliation></author></analytic><series><title level="j">Neurotoxicity research</title><idno type="eISSN">1476-3524</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">β-Methylamino-L-alanine (BMAA) is implicated in neurodegeneration and neurotoxicity, particularly in ALS-Parkinson Dementia Complex. Neurotoxic properties of BMAA have been partly elucidated, while its transcellular spreading capacity has not been examined. Using reconstructed neuronal networks in microfluidic chips, separating neuronal cells into two subcompartments-(1) the proximal, containing first-order neuronal soma and dendrites, and (2) a distal compartment, containing either only axons originating from first-order neurons or second-order striatal neurons-creates a cortico-striatal network. Using this system, we investigated the toxicity and spreading of BMAA in murine primary neurons. We used a newly developed antibody to detect BMAA in cells. After treatment with 10 μM BMAA, the cyanotoxin was incorporated in first-degree neurons. We also observed a rapid trans-neuronal spread of BMAA to unexposed second-degree neurons in 48 h, followed by axonal degeneration, with limited somatic death. This in vitro study demonstrates BMAA axonal toxicity at sublethal concentrations and, for the first time, the transcellular spreading abilities of BMAA. This neuronal dying forward spread that could possibly be associated with progression of some neurodegenerative diseases especially amyotrophic lateral sclerosis.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement></list><tree><country name="Australie"><noRegion><name sortKey="Tan, Vanessa X" sort="Tan, Vanessa X" uniqKey="Tan V" first="Vanessa X" last="Tan">Vanessa X. Tan</name></noRegion><name sortKey="Guillemin, Gilles J" sort="Guillemin, Gilles J" uniqKey="Guillemin G" first="Gilles J" last="Guillemin">Gilles J. Guillemin</name><name sortKey="Lim, Chai K" sort="Lim, Chai K" uniqKey="Lim C" first="Chai K" last="Lim">Chai K. Lim</name></country><country name="France"><region name="Île-de-France"><name sortKey="Lassus, Benjamin" sort="Lassus, Benjamin" uniqKey="Lassus B" first="Benjamin" last="Lassus">Benjamin Lassus</name></region><name sortKey="Bessede, Alban" sort="Bessede, Alban" uniqKey="Bessede A" first="Alban" last="Bessede">Alban Bessede</name><name sortKey="Courte, Josquin" sort="Courte, Josquin" uniqKey="Courte J" first="Josquin" last="Courte">Josquin Courte</name><name sortKey="Peyrin, Jean Michel" sort="Peyrin, Jean Michel" uniqKey="Peyrin J" first="Jean-Michel" last="Peyrin">Jean-Michel Peyrin</name><name sortKey="Tixador, Philippe" sort="Tixador, Philippe" uniqKey="Tixador P" first="Philippe" last="Tixador">Philippe Tixador</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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