Abstract
The non-proteinogenic amino acid beta-methyl-amino-l-alanine (BMAA) is a neurotoxin produced by cyanobacteria. BMAA accumulation in the brain of animals via biomagnification along the food web can contribute to the development of neurodegenerative diseases such as Amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC), the latter being associated with a loss of dopaminergic neurons. Daphnia magna is an important microcrustacean zooplankton species that plays a key role in aquatic food webs, and BMAA-producing cyanobacteria often form part of their diet. Here, we tested the effects of BMAA on putative neurodegeneration of newly identified specific dopaminergic neurons in the optic ganglia/brain complex of D. magna using quantitative tyrosine-hydroxylase immunohistochemistry and fluorescence cytometry. The dopaminergic system was analysed in fed and starved isogenic D. magna adults incubated under different BMAA concentrations over 4 days. Increased BMAA concentration showed significant decrease in the stainability of dopaminergic neurons of D. magna, with fed animals showing a more extreme loss. Furthermore, higher BMAA concentrations tended to increase offspring mortality during incubation. These results are indicative of ingested BMAA causing neurodegeneration of dopaminergic neurons in D. magna and adversely affecting reproduction. This may imply similar effects of BMAA on known human neurodegenerative diseases involving dopaminergic neurons.
Highlights
The non-proteinogenic amino acid β-methyl-amino-L-alanine (BMAA), was first identified from the seeds of Cycas trees on the island of Guam in the Pacific Ocean linked as a causative agent to the high incidence of amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS-PDC) among many of the indigenous Chamorro people of this island [1,2,3]
A system of 25–27 paired dopaminergic neurons have been mapped in the optic
Complex a systemofofD.25–27 neurons have been some mapped in theofoptic ganglia/brain magnapaired
Summary
The non-proteinogenic amino acid β-methyl-amino-L-alanine (BMAA), was first identified from the seeds of Cycas trees on the island of Guam in the Pacific Ocean linked as a causative agent to the high incidence of amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS-PDC) among many of the indigenous Chamorro people of this island [1,2,3]. The cyanobacterium Nostoc living symbiotically with cycad trees was identified as the source for BMAA [2]. Another extensive source for BMAA was discovered in the skin of flying foxes, which devour large amounts of Cycas seeds and are Toxins 2018, 10, 527; doi:10.3390/toxins10120527 www.mdpi.com/journal/toxins. Several potential mechanisms by which environmental exposure to BMAA can lead to such neurological disorders have been proposed [6,7,8] and which are caused by neurodegeneration [9,10,11].
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