Detection of the Cyanotoxins L-BMAA Uptake and Accumulation in Primary Neurons and Astrocytes
Neurotox Res. 2017-08-30; 33(1): 55-61
DOI: 10.1007/s12640-017-9787-9
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https://www.bordeaux-neurocampus.fr/12186
1. Neurotox Res. 2018 Jan;33(1):55-61. doi: 10.1007/s12640-017-9787-9. Epub 2017
Aug 30.
Detection of the Cyanotoxins L-BMAA Uptake and Accumulation in Primary Neurons
and Astrocytes.
Tan VX(1), Mazzocco C(2), Varney B(1), Bodet D(2), Guillemin TA(1), Bessede
A(2), Guillemin GJ(3)(4).
Author information:
(1)Macquarie University Centre for MND Research, Department of Biological
Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney,
NSW, 2109, Australia.
(2)ImmuSmol, Pessac, France.
(3)Macquarie University Centre for MND Research, Department of Biological
Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney,
NSW, 2109, Australia. .
(4)Neuroinflammation Group, Faculty of Medicine and Health Sciences, Macquarie
University, Sydney, NSW, 2109, Australia. .
We show for the first time that a newly developed polyclonal antibody (pAb) can
specifically target the cyanotoxin β-methylamino-L-alanine (BMAA) and can be
used to enable direct visualization of BMAA entry and accumulation in primary
brain cells. We used this pAb to investigate the effect of acute and chronic
accumulation, and toxicity of both BMAA and its natural isomer
2,4-diaminobutyric acid (DAB), separately or in combination, on primary cultures
of rat neurons. We further present evidence that co-treatment with BMAA and DAB
increased neuronal death, as measured by MAP2 fluorescence level, and appeared
to reduce BMAA accumulation. DAB is likely to be acting synergistically with
BMAA resulting in higher level of cellular toxicity. We also found that glial
cells such as microglia and astrocytes are also able to directly uptake BMAA
indicating that additional brain cell types are affected by BMAA-induced
toxicity. Therefore, BMAA clearly acts at multiple cellular levels to possibly
increase the risk of developing neurodegenerative diseases, including neuro- and
gliotoxicity and synergetic exacerbation with other cyanotoxins.
DOI: 10.1007/s12640-017-9787-9
PMID: 28852990 [Indexed for MEDLINE]