Premium
Endogenous reductions in N ‐methyl‐ d ‐aspartate receptor activity inhibit nitric oxide production in the anoxic freshwater turtle cortex
Author(s) -
Pamenter Matthew Edward,
Hogg David William,
Buck Leslie Thomas
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.04.041
Subject(s) - nmda receptor , nitric oxide , anoxic waters , excitotoxicity , glutamatergic , endogeny , chemistry , glutamate receptor , receptor , cortex (anatomy) , biology , biochemistry , endocrinology , neuroscience , environmental chemistry
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.