New perspectives on the mechanisms through which nitric oxide may affect learning and memory processes.
Nitric oxide (NO) has been well established as a molecule necessary for memory consolidation. Interestingly, the majority of research has focused on only a single mechanism through which NO acts, namely the up-regulation of guanylate cyclase (GC). However, since NO and NO-derived reactive nitrogen species are capable of interacting with a broad array of enzymes, ion channels and receptors, a singular focus on GC appears short-sighted. Although NO inhibits the action of a number of molecules there are four, in addition to GC, which are up-regulated by the direct presence of NO, or NO-derived radicals, and implicated in memory processing. They are: cyclic nucleotide-gated channels; large conductance calcium-activated potassium channels; ryanodine receptor calcium release (RyR) channels; and the enzyme mono(ADP-ribosyl) transferase. This review presents evidence that not only are these four molecules worthy of investigation as GC-independent mechanisms through which NO may act, but that behavioural evidence already exists suggesting a relationship between NO and the RyR channel.
Edwards
T M
TM
School of Psychology, Psychiatry and Psychological Medicine, Monash University-Clayton, Wellington Road, Clayton, 3800 Vic., Australia. tom.edwards@med.monash.edu.au
Rickard
N S
NS
D000818:Animals; D001921:Brain / Q000502:physiology*; D006801:Humans; D007473:Ion Channels; D007858:Learning / Q000502:physiology*; D008568:Memory / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology*; D015290:Second Messenger Systems / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D007473:Ion Channels; D009569:Nitric Oxide