BMAA selectively injures motor neurons via AMPA/kainate receptor activation

Rao, Shyam; Banack, Sandra Anne; Cox, Paul Alan; Weiss, John H.

doi:10.1016/j.expneurol.2006.04.017

Cited by 246 publications

(136 citation statements)

References 68 publications

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“…A recent report has shown that BMAA concentrations as low as 30 µM can cause selective death of motor neurons (Rao et al, 2006). This study suggests that in contrast to cortical neurons, motor neurons are highly susceptible to BMAA toxicity even without an additional insult.…”

Section: Discussionmentioning

confidence: 72%

β-N-methylamino-l-alanine enhances neurotoxicity through multiple mechanisms

Lobner

Piana

Salous

et al. 2007

Neurobiology of Disease

238

136

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The idea that the environmental toxin β-N-methylamino-L-alanine (BMAA) is involved in neurodegenerative diseases on Guam has risen and fallen over the years. The theory has gained greater interest with recent reports that BMAA is biomagnified, is widely distributed around the planet, and is present in the brains of Alzheimer's patients in Canada. We provide two important new findings. First, we show that BMAA at concentrations as low as 10 µM can potentiate neuronal injury induced by other insults. This is the first evidence that BMAA at concentrations below the mM range can enhance death of cortical neurons and illustrates potential synergistic effects of environmental toxins with underlying neurological conditions. Second, we show that the mechanism of BMAA toxicity is three fold: it is an agonist for NMDA and mGluR5 receptors, and induces oxidative stress. The results provide further support for the hypothesis that BMAA plays a role in neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 72%

β-N-methylamino-l-alanine enhances neurotoxicity through multiple mechanisms

Lobner

Piana

Salous

et al. 2007

Neurobiology of Disease

238

136

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“…Confirmation through five different techniques that BMAA is produced by the marine Nostoc species represented by the CCMED-01 samples increases our interest in finding out if this potent neurotoxin, which selectively targets motor neurons [13,14], can be biomagnified within marine ecosystems. We await with interest the results of ongoing studies of BMAA biomagnification at the University of Hawaii, Stockholm University, Chiba University, and our Institute designed to test this possibility.…”

Section: Discussionmentioning

confidence: 99%

Production of the Neurotoxin BMAA by a Marine Cyanobacterium

Banack

2007

Mar. Drugs

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“…It has been demonstrated that BMAA activates different types of glutamate receptors in diverse brain areas (Spencer et al, 1987;Copani et al, 1990Copani et al, , 1991Allen et al, 1993;Pai et al, 1993;Staton and Bristow, 1998;Rao et al, 2006;Lobner et al, 2007). To this regard, we aimed to explore its effect onto the "secondary" cells of the SNpc, presumably GABAergic neurons ( Fig.…”

Section: Bmaa Activates Ampa Receptors In Gabaergic Neurons Of the Snpcmentioning

confidence: 99%

“…This creates an endogenous reservoir of neurotoxin within the human body, capable of slow release into cerebral and other tissues during protein catabolism for years or decades after its consumption. In vivo (Spencer et al, 1987;Smith and Meldrum, 1990;Rakonczay et al, 1991;Chang et al, 1993;Santucci et al, 2009) and in vitro studies have reported that BMAA acts as a glutamate agonist onto spinal motoneurons (Rao et al, 2006) and cortical (Lobner et al, 2007) and cerebellar (Staton and Bristow, 1997) neurons. However, a detailed description of its actions on substantia nigra pars compacta (SNpc) dopaminergic cells (DAergic) is still lacking.…”

Section: Introductionmentioning

confidence: 99%

Metabotropic Glutamate Receptor 1 Mediates the Electrophysiological and Toxic Actions of the Cycad Derivative β-N-Methylamino-l-Alanine on Substantia Nigra Pars Compacta DAergic Neurons

et al. 2010

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Amyotrophic lateral sclerosis-Parkinson dementia complex (ALS-PDC) is a neurodegenerative disease with ALS, parkinsonism, andAlzheimer's symptoms that is prevalent in the Guam population. ␤-N-Methylamino alanine (BMAA) has been proposed as the toxic agent damaging several neuronal types in ALS-PDC, including substantia nigra pars compacta dopaminergic (SNpc DAergic) neurons. BMAA is a mixed glutamate receptor agonist, but the specific pathways activated in DAergic neurons are not yet known. We combined electrophysiology, microfluorometry, and confocal microscopy analysis to monitor membrane potential/current, cytosolic calcium concentration (

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BMAA selectively injures motor neurons via AMPA/kainate receptor activation

Cited by 246 publications

References 68 publications

β-N-methylamino-l-alanine enhances neurotoxicity through multiple mechanisms

β-N-methylamino-l-alanine enhances neurotoxicity through multiple mechanisms

Production of the Neurotoxin BMAA by a Marine Cyanobacterium

Metabotropic Glutamate Receptor 1 Mediates the Electrophysiological and Toxic Actions of the Cycad Derivative β-N-Methylamino-l-Alanine on Substantia Nigra Pars Compacta DAergic Neurons

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