Neurotoxicity ofβ-N-methylamino-l-alanine (BMAA) andβ-N-oxalylamino-l-alamine (BOAA) on cultured cortical neurons

  title={Neurotoxicity of$\beta$-N-methylamino-l-alanine (BMAA) and$\beta$-N-oxalylamino-l-alamine (BOAA) on cultured cortical neurons},
  author={John H Weiss and Jae-Young Koh and Dennis W. Choi},
  journal={Brain Research},

Acute β-N-Methylamino-L-alanine Toxicity in a Mouse Model

The presumptive median lethal dose (LD50), the Lowest-Observed-Adverse-Effect Level (LOAEL), and histopathologic lesions caused by the naturally occurring BMAA isomer, L-BMAA, in mice were determined.

β-N-Methylamino-l-alanine (BMAA) perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells as determined by metabolic profiling

The results indicate that BMAA can interfere with metabolic pathways involved in neurotransmission in human neuroblastoma cells, with significant perturbations in protein biosynthesis, amino acid metabolism pathways and citrate cycle.

Mechanisms of β-N-methylamino-L-alanine induced neurotoxicity

  • D. Lobner
  • Biology
    Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases
  • 2009
Through its effect of system xc-, BMAA can induce oxidative stress and increase extracellular glutamate, which provides an attractive mechanism for the multiple neurological deficits that BMAA has been implicated in inducing.

BMAA – an unusual cyanobacterial neurotoxin

  • Kaivalya J VyasJ. Weiss
  • Biology
    Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases
  • 2009
While BMAA is a weal agonist at NMDA-type glutamate receptors, low levels of BMAA are found to selectively damage vulnerable sub-populations of neurons, including motor neurons, via activation of AMPA/kainate receptors.



Beta-N-methylamino-L-alanine neurotoxicity: requirement for bicarbonate as a cofactor.

Ingestion of the excitotoxic cycad seed amino acid beta-N-methylamino-L-alanine may be responsible for the neuronal degeneration associated with Guam amyotrophic lateral

Discovery and partial characterization of primate motor-system toxins.

BOAA and BMAA are the first members of the excitotoxin family to have been shown to possess chronic motor-system toxic potential and provide a rational basis for searching for comparable endogenous neurotoxins in sporadic and inherited forms of human motor neuron disease.

Brain and retinal damage from lathyrus excitotoxin, β-N-oxalyl-L-α,β-diaminopropionic acid

It is reported that ODAP, administered intraperitoneally to immature mice, induces lesions in the retina, hypothalamus and lower medulla, similar to that demonstrated in animals after oral or subcutaneous administration of glutamate (Glu).

Neurons containing NADPH-diaphorase are selectively resistant to quinolinate toxicity.

The results support the hypothesis that the disease may be caused by excess exposure to quinolinate or some other endogenous N-methyl-D-aspartate agonist, and suggest neurons containing NADPH-d may have an unusual distribution of receptors for excitatory amino acids.

L-Glutamate has higher affinity than other amino acids for [3H]-D-AP5 binding sites in rat brain membranes

It is reported that [3H]-D-AP5 binds specifically to rat brain membranes, that the hippocampus and cerebral cortex are enriched in these sites relative to other brain areas and that L-glutamate has higher affinity for these receptors than have all other transmitter candidates tested.

Central Effects of β-N-Oxalyl-α,β-diaminopropionic Acid and other Lathyrus Factors

Investigation has been made of the action of toxic substances present in Lathyrus species responsible for human neurolathyrism on single nerve cells of cats anaesthetized with pentobarbitone and the degree of susceptibility to these toxic agents varies between different animal species.

Vulnerability of cultured cortical neurons to damage by excitotoxins: differential susceptibility of neurons containing NADPH-diaphorase

  • JY KohD. Choi
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1988
The hypothesis that neuronal loss in Huntington's disease might result from excessive NMDA- receptor stimulation by any selective NMDA agonist is supported.