Endogenous reductions in N-methyl-d-aspartate receptor activity inhibit nitric oxide production in the anoxic freshwater turtle cortex.
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.
Pamenter
Matthew Edward
ME
Department of Cellular and Systems Biology, University of Toronto, ON, Canada M5S 3G5. matt.pamenter@utoronto.ca
Hogg
David William
DW
Buck
Leslie Thomas
LT
D000693:Anaerobiosis; D000818:Animals; D002540:Cerebral Cortex / Q000098:blood supply* / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D009569:Nitric Oxide / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D010100:Oxygen / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D014426:Turtles / Q000378:metabolism*
D016194:Receptors, N-Methyl-D-Aspartate; D009569:Nitric Oxide; D010100:Oxygen