Interaction between ß-N-methylamino- l-alanine and excitatory amino acid receptors in brain slices and neuronal cultures
References (31)
- et al.
Inhibition of [3H]α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic binding by the excitotoxin ß-N-oxalyl- l-α,ß-diaminopropionic acid
Eur. J. Pharmacol.
(1988) - et al.
l-[3H]Glutamate labels the metabotropic excitatory amino acid receptor in rodent brain
Neurosci. Lett.
(1990) Calcium-mediated neurotoxicity: relationship to specific channel types and role in ischemic damage
Trends Neurosci.
(1988)- et al.
Beta-N-methylamino-l-alanine (l-BMAA) is a potent agonist of ‘metabolotropic’ glutamate receptors
Eur. J. Pharmacol.
(1990) - et al.
CPP, a new potent and selective NMDA antagonis. Depression of central neuron response, affinity for [3H]d-AP-5 binding sites on brain membranes and anticonvulsant activity
Brain Research
(1986) - et al.
Freezing elminates a specific population ofl-glutamate receptors in synaptic membranes
Neurosci. Lett.
(1983) - et al.
Inhibition of phosphoinositide hydrolysis by the novel neurotoxin ß-N-oxalyl- l-α,ß-aminoproprionic acid (l-BOAA)
Brain Research
(1990) - et al.
Trans-ACPD, a selective agonist of phosphoinositide-coupled excitatory amino acid receptors
Eur. J. Pharmacol.
(1989) - et al.
Specific antagonism of excitotoxic action of ‘uncommon’ amino acids assayed in organotypic mouse cortical cultures
Brain Research
(1987) - et al.
A new mechanism for glutamate receptor action: phosphoinositide hydrolysis
Trends Neurosci.
(1988)
Lathyrism: evidence for role of the neuroexcitatory amino acid BOAA
Lancet
(1986)
Bicarbonate dependence of glutamate receptor activation byß-N-methyl-amino-l-alanine: channel recording and study with related compounds
Neuron
(1989)
Neurotoxicity ofß-N-methylamino-l-alanine (BMAA) andß-N-oxalylamino-l-alanine (BOAA) on cultured cortical neurons
Brain Research
(1989)
Different coupling of excitatory amino acid receptors with Ca2+ channels in primary cultures of granule cells
Neuropharmacology
(1985)
AP3 andl-BMAA displace [3H]glutamate binding to the metabotropic receptor
Cited by (64)
Degradation mechanisms of cyanobacteria neurotoxin β-N-methylamino-L-alanine (BMAA) during UV<inf>254</inf>/H<inf>2</inf>O<inf>2</inf> process: Kinetics and pathways
2022, ChemosphereCitation Excerpt :β-N-methylamino-l-alanine (BMAA), a kind of cyanotoxin, has been considered as a possible cause of neurodegenerative diseases (Copani et al., 1991).
Degradation of neurotoxin β-N-methylamino-L-alanine by UV<inf>254</inf> activated persulfate: Kinetic model and reaction pathways
2021, Chemical Engineering JournalEvaluating amino acids as protectants against β-N-methylamino-L-alanine-induced developmental neurotoxicity in a rat model
2020, Toxicology and Applied Pharmacology
Copyright © 1991 Published by Elsevier B.V.