Prolonged pre-exposure to 1-aminocyclopropanecarboxylic acid protects against subsequent glutamate toxicity in vitro.
Sustained 20 h pre-exposure to 1 mM 1-aminocyclopropanecarboxylic acid (ACPC, which was removed 30 min before addition of 25 microM glutamate) significantly reduced the subsequent neurotoxicity of glutamate in cultured forebrain and cerebellar neurons. The magnitude of neuronal protection was further enhanced if the neurons pretreated with ACPC were re-exposed to ACPC during glutamate challenge. These results closely resemble earlier findings with cultured spinal cord neurons and indicate that these primary cell culture preparations might be suitable for the assessment of the mechanism(s) underlying chronic ACPC-induced modification of the NMDA receptor complex.
Lin
Y
Y
Division of Neurosciences, Walter Reed Army Institute of Research, Washington, DC 20307, USA.
Long
J B
JB
D000596:Amino Acids / Q000494:pharmacology*; D000598:Amino Acids, Cyclic; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D002531:Cerebellum / Q000166:cytology / Q000187:drug effects; D018698:Glutamic Acid / Q000633:toxicity*; D009474:Neurons / Q000166:cytology / Q000187:drug effects*; D016548:Prosencephalon / Q000166:cytology / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley
D000596:Amino Acids; D000598:Amino Acids, Cyclic; C023863:1-aminocyclopropane-1-carboxylic acid; D018698:Glutamic Acid