Abstract：
:beta-N-Oxalylamino-L-alanine (BOAA) and beta-N-methylamino-L-alanine (BMAA) were tested for their ability to produce acute excitotoxicity in in embryonic chick retina. gamma-Aminobutyric acid (GABA) release and histology were monitored in retina treated with various concentrations of BOAA, BMAA, kainate (KA), N-methyl-D-aspartate (NMDA), or glutamate. BOAA and BMAA caused retinal lesions similar to those produced by the excitatory amino acids. BOAA was slightly less potent than KA, whereas BMAA had a potency similar to glutamate. BOAA, like KA and NMDA, caused a dose-dependent increase in GABA release. Addition of the NMDA antagonist (+)-MK-801, completely blocked acute excitotoxicity caused by NMDA or BMAA but was ineffective against KA or BOAA. Kynurenate, a nonspecific glutamate receptor antagonist, and DIDS, a Cl- channel blocker, were effective in blocking all agonist-induced toxicity. It is concluded that BOAA and BMAA cause excitotoxic damage in retina; BOAA induces toxicity through a non-NMDA type glutamate receptor and BMAA through the NMDA receptor.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Zeevalk GD,Nicklas WJdoi
10.1016/0304-3940(89)90093-1subject
Has Abstractpub_date
1989-07-31 00:00:00pages
284-90issue
2-3eissn
0304-3940issn
1872-7972pii
0304-3940(89)90093-1journal_volume
102pub_type
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