Endogenous reductions in N-methyl-d-aspartate receptor activity inhibit nitric oxide production in the anoxic freshwater turtle cortex |
| |
Authors: | Pamenter Matthew Edward Hogg David William Buck Leslie Thomas |
| |
Affiliation: | Department of Cellular and Systems Biology, University of Toronto, ON, Canada M5S 3G5. matt.pamenter@utoronto.ca |
| |
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: | APV, smallcaps" >dl-2-amino-5-phosphonopentanoic acid CBF, cerebral blood flow DAF-FM, 4-amino-5-methylamino-2′,7′-difluorofluorescein ECD, excitotoxic cell death smallcaps" >l-NAME, NG-nitro- smallcaps" >l-arginine methyl ester NMDAR, N-methyl- smallcaps" >d-aspartate receptor nNOS, neuronal nitric oxide synthase NO, nitric oxide NOS, nitric oxide synthase PSD-95, Post-synaptic density 95 ROS, reactive oxygen species SNP, sodium nitroprusside dihydrate |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|