Nitric oxide-dependent long-term potentiation is blocked by a specific inhibitor of soluble guanylyl cyclase

摘要: The diffusible second messenger, nitric oxide, is synthesised in central neurons response to activation of glutamate receptors or other stimuli that increase cytosolic Ca2+ concentrations. Among the many roles suggested for oxide nervous system mediating synaptic plasticity. For example, long-term potentiation CA1 region rat hippocampus was reported be blocked by inhibitors synthase and exogenous has been claimed induce an enduring enhancement strength under certain conditions. These findings, however, are controversial even when a participation evident, transduction mechanism unclear. A well-known action stimulate soluble form guanylyl cyclase, thereby evoking accumulation cyclic GMP target cells but several mechanisms have proposed, including stimulation ADP ribosyltransferase cyclooxygenase, nitrosylation protein thiol residues. identification selective inhibitor oxadiazoloquinoxaline derivative, ODQ, provides, first time, means investigate importance pathway signal transduction. We find ODQ inhibitor, nitroarginine, reduce hippocampal equal mutually exclusive manner, suggesting actions this phenomenon entirely mediated through GMP. experiments also show there component involves neither nor