Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2049014 | FEBS Letters | 2008 | 5 Pages |
Abstract
Increased nitric oxide (NO) production from hypoxic mammalian neurons increases cerebral blood flow (CBF) but also glutamatergic excitotoxicity and DNA fragmentation. Anoxia-tolerant freshwater turtles have evolved NO-independent mechanisms to increase CBF; however, the mechanism(s) of NO regulation are not understood. In turtle cortex, anoxia or NMDAR blockade depressed NO production by 27 ± 3% and 41 ± 5%, respectively. NMDAR antagonists also reduced the subsequent anoxic decrease in NO by 74 ± 6%, suggesting the majority of the anoxic decrease is due to endogenous suppression of NMDAR activity. Prevention of NO-mediated damage during the transition to and from anoxia may be incidental to natural reductions of NMDAR activity in the anoxic turtle cortex.
Keywords
nNOS4-Amino-5-methylamino-2′,7′-difluorofluoresceinpost-synaptic density 95NG-nitro-l-arginine methyl esterDAF-FMexcitotoxic cell deathNMDARAPVPSD-95NOSECDCBFl-NAMEROSDL-2-Amino-5-phosphonopentanoic acidcerebral blood flowchannel arrestdiaminofluoresceinneuronal nitric oxide synthaseNitric oxidenitric oxide synthaseHypoxiaSNPCalciumReactive oxygen speciesN-methyl-d-aspartate receptor
Related Topics
Life Sciences
Agricultural and Biological Sciences
Plant Science
Authors
Matthew Edward Pamenter, David William Hogg, Leslie Thomas Buck,