Abstract:
:Prolonged activation of brain N-methyl-D-aspartic acid (NMDA) receptors increases intraneuronal (Ca2+) and nitric oxide (NO) synthesis, and may be responsible for neuronal death in acute brain insults and chronic neurodegenerative diseases. NO can be converted in vitro to toxic hydroxyl (OH) radical. Using microdialysis of striatum in awake animals, we found that local NMDA receptor activation increased outflow of OH radicals four-fold. NMDA-stimulated OH production was blocked by inhibitors of nitric oxide synthase (NOS) and protein kinase C (PKC). NMDA receptor-mediated neuronal death may derive from NOS- and PKC-dependent synthesis of OH radicals.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Hammer B,Parker WD Jr,Bennett JP Jrdoi
10.1097/00001756-199310000-00018subject
Has Abstractpub_date
1993-10-25 00:00:00pages
72-4issue
1eissn
0959-4965issn
1473-558Xjournal_volume
5pub_type
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