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Long‐term depression (LTD) of synaptic strength is induced by glutamate‐triggered increases in postsynaptic [Ca²⁺], through either influx or release from intracellular stores. Induction of LTD has also been reported to require release of Ca²⁺ from presynaptic stores and activation of presynaptic Ca²⁺/calmodulin‐dependent protein kinase II. This finding leads to the hypothesis that the intercellular messenger nitric oxide (NO) may be a means by which postsynaptic Ca²⁺ triggers changes expressing LTD in presynaptic terminals. We report that bath application of the oxadiazoloquinoxalone derivative ODQ (5 μM), a selective inhibitor of NO‐sensitive guanylyl cyclase (NOGC), markedly attenuated (90%) the magnitude of LTD induced by low‐frequency stimulation (LFS; 1 Hz/15 min) of Schaffer collateral‐CA1 synapses in hippocampal slices in vitro. Both the NO donor S‐nitroso‐N‐acetylpenicillamine (100 μM) and …