title: Endogenous reductions in N-methyl-d-aspartate receptor activity inhibit nitric oxide production in the anoxic freshwater turtle cortex.
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.
authors.affiliation: Department of Cellular and Systems Biology, University of Toronto, ON, Canada M5S 3G5. matt.pamenter@utoronto.ca
authors.forename: Matthew Edward
authors.initials: ME
authors.lastname: Pamenter
authors.forename: David William
authors.initials: DW
authors.lastname: Hogg
authors.forename: Leslie Thomas
authors.initials: LT
authors.lastname: Buck
mesh_terms: 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*
chemical_list: D016194:Receptors, N-Methyl-D-Aspartate; D009569:Nitric Oxide; D010100:Oxygen