Electrophysiological Effect of β‐N‐Methylamino‐L‐Alanine on Retzius Nerve Cells of the Leech <i>Haemopis sanguisuga</i>

Nedeljkov, Vladimir; Lopičić, Srdjan; Pavlović, Dragan; Cemerikic, Dusan

doi:10.1196/annals.1342.034

Cited by 12 publications

(6 citation statements)

References 6 publications

(6 reference statements)

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“…36 Nedeljkov et al investigated the effects of L-BMAA on Retzius nerve cells of isolated ganglia of the leech Haemopis sanguisuga and showed that the presence of bicarbonate ions produces a 4-fold increase in BMAA-induced depolarization of the membrane potential. 37 Lopicic and colleagues, using the same model, reported that application of both 1 mmol L -1 L-BMAA in Ringer solution containing 20 mmol L -1 bicarbonate caused a significant 74 % decrease in the input resistance of directly polarized membrane and that the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration of 100 μmol L -1 decreased the effect of L-BMAA on membrane potential by 57 %. The authors also presented evidence for a rise in the intracellular Na + concentration (Na + ) c and decrease in the intracellular K + concentration (K + ) c during BMAA induced depolarizations.…”

Section: Mechanisms Of Bmaa Neurotoxicitymentioning

confidence: 97%

Excitatory amino acid beta-N-methylamino-L-alanine is a putative environmental neurotoxin

Lopičić

Stanojević

Pathak

et al. 2011

JSCS

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The amino acid β-N-methylamino-L-alanine (L-BMAA) has been associated with the amyotrophic lateral sclerosis/parkinsonism-dementia complex in three distinct western Pacific populations. The putative neurotoxin is produced by cyanobacteria, which live symbiotically in the roots of cycad trees. L-BMAA was thought to be a threat only to those few populations whose diet and medicines rely heavily on cycad seeds. However, the recent discovery that cyanobacteria from diverse terrestrial, freshwater, and saltwater ecosystems around the world produce the toxin requires a reassessment of whether it poses a larger health threat. Therefore, it is proposed that monitoring L-BMAA levels in cyanobacteria-contaminated water supplies might be prudent.

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Section: Mechanisms Of Bmaa Neurotoxicitymentioning

confidence: 97%

Excitatory amino acid beta-N-methylamino-L-alanine is a putative environmental neurotoxin

Lopičić

Stanojević

Pathak

et al. 2011

JSCS

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“…[73] measured the membrane input resistance of the nerve cells of the leech Haemopis sanguisuga after treatment with BMAA (100 μM–10 mM) and HCO 3 − (20 mM). A significant reduction in input membrane resistance was measured, indicating that BMAA depolarizes the cell by increasing membrane permeability and conductance.…”

Section: Summary Of the Multiple Mechanisms Of Bmaa Activitymentioning

confidence: 99%

“…The physiological concentrations of bicarbonate ions (10 mM and above) reacts with BMAA to form a β-carbamate [60]. In this form, BMAA can compete in binding various glutamate receptors, such as NMDA receptors [55,56,64,65], AMPA receptors [55,56], and metabotropic and ionotropic glutamate receptors [65,73,81,84] (Figure 3i). Activation of the various glutamate receptors leads to shifts in cellular ion concentrations resulting in increases in Na + [81] and Ca 2+ [70,76,84], and a decrease in K + [81] concentrations (Figure 3ii).…”

Section: A Summary Of the Mode Of Action Of Bmaa Based On The Currmentioning

confidence: 99%

“…Activation of the various glutamate receptors leads to shifts in cellular ion concentrations resulting in increases in Na + [81] and Ca 2+ [70,76,84], and a decrease in K + [81] concentrations (Figure 3ii). Activation also causes the cell to become depolarised [73] leading to permeabilisation of the cell membrane, resulting in the release of noradrenalin [64] (Figure 3iii). BMAA also inhibits the cysteine/glutamate antiporter system Xc − [77] (Figure 3iv), preventing the uptake of cysteine, resulting in glutathione depletion, which contributes to increases in oxidative stress.…”

Section: A Summary Of the Mode Of Action Of Bmaa Based On The Currmentioning

confidence: 99%

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Does α-Amino-β-methylaminopropionic Acid (BMAA) Play a Role in Neurodegeneration?

Chiu

Gehringer

Welch

et al. 2011

IJERPH

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The association of α-amino-β-methylaminopropionic acid (BMAA) with elevated incidence of amyotrophic lateral sclerosis/Parkinson’s disease complex (ALS/PDC) was first identified on the island of Guam. BMAA has been shown to be produced across the cyanobacterial order and its detection has been reported in a variety of aquatic and terrestrial environments worldwide, suggesting that it is ubiquitous. Various in vivo studies on rats, mice, chicks and monkeys have shown that it can cause neurodegenerative symptoms such as ataxia and convulsions. Zebrafish research has also shown disruption to neural development after BMAA exposure. In vitro studies on mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca2+ influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. The current review pertaining to the neurotoxicity of BMAA clearly demonstrates its ability to adversely affect neural tissues, and implicates it as a potentially significant compound in the aetiology of neurodegenerative disease. When considering the potential adverse health effects upon exposure to this compound, further research to better understand the modes of toxicity of BMAA and the environmental exposure limits is essential.

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“…Extensive in vitro experiments have demonstrated that the neurotoxicity of BMAA for neurons is a result of multiple mechanisms including action at NMDA ( N -methyl- d -aspartic acid) or AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)/kainate receptors, generation of ROS (reactive oxygen species), and production of excessive dopamine [3,4,5,6,7]. Recent reports have documented that BMAA inhibited antioxidant enzymes of the macrophyte Ceratophyllum demersum and of aquatic plants ( Lomariopsis lineata , Fontinalis antipyretica , Riccia fluitans , and Taxiphyllum barbieri ), indirectly implicating the induction of oxidative stress in plants by BMAA [8,9].…”

Section: Introductionmentioning

confidence: 99%

New Typical Vector of Neurotoxin β-N-Methylamino-l-Alanine (BMAA) in the Marine Benthic Ecosystem

Song

et al. 2016

Marine Drugs

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The neurotoxin β-N-methylamino-l-alanine (BMAA) has been identified as an environmental factor triggering neurodegenerative diseases such as Amyotrophic Lateral Sclerosis (ALS) and Alzheimer’s disease (AD). We investigated the possible vectors of BMAA and its isomers 2,4-diaminobutyric acid (DAB) and N-2(aminoethyl)glycine (AEG) in marine mollusks collected from the Chinese coast. Sixty-eight samples of marine mollusks were collected along the Chinese coast in 2016, and were analyzed by an HILIC-MS/MS (hydrophilic interaction liquid chromatography with tandem quadrupole mass spectrometer) method without derivatization. BMAA was detected in a total of five samples from three species: Neverita didyma, Solen strictus, and Mytilus coruscus. The top three concentrations of free-form BMAA (0.99~3.97 μg·g−1 wet weight) were detected in N. didyma. DAB was universally detected in most of the mollusk samples (53/68) with no species-specific or regional differences (0.051~2.65 μg·g−1 wet weight). No AEG was detected in any mollusk samples tested here. The results indicate that the gastropod N. didyma might be an important vector of the neurotoxin BMAA in the Chinese marine ecosystem. The neurotoxin DAB was universally present in marine bivalve and gastropod mollusks. Since N. didyma is consumed by humans, we suggest that the origin and risk of BMAA and DAB toxins in the marine ecosystem should be further investigated in the future.

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Electrophysiological Effect of β‐N‐Methylamino‐L‐Alanine on Retzius Nerve Cells of the Leech Haemopis sanguisuga

Cited by 12 publications

References 6 publications

Excitatory amino acid beta-N-methylamino-L-alanine is a putative environmental neurotoxin

Excitatory amino acid beta-N-methylamino-L-alanine is a putative environmental neurotoxin

Does α-Amino-β-methylaminopropionic Acid (BMAA) Play a Role in Neurodegeneration?

New Typical Vector of Neurotoxin β-N-Methylamino-l-Alanine (BMAA) in the Marine Benthic Ecosystem

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