Abstract:
:Excessive activation of the N-methyl-D-aspartate (NMDA) receptor-channel complex has been implicated as one of the mechanisms by which ischemia-induced neuronal damage is mediated. Elevated glycine levels during ischemia may contribute to damage mediated by the NMDA receptor as glycine binding potentiates NMDA responses, and may be necessary for channel opening. We investigated the protective effects of 7-chlorokynurenic acid--a competitive antagonist at the glycine binding site associated with the NMDA receptor--against hippocampal CA1 cell loss induced by transient forebrain ischemia in rats. Intraventricular administration of the drug immediately before the onset of ischemia significantly attenuated neuronal loss compared to vehicle-treated animals.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Wood ER,Bussey TJ,Phillips AGdoi
10.1016/0304-3940(92)90191-9keywords:
subject
Has Abstractpub_date
1992-09-28 00:00:00pages
10-4issue
1eissn
0304-3940issn
1872-7972pii
0304-3940(92)90191-9journal_volume
145pub_type
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journal_title:Neuroscience letters
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