Reactive oxygen species (ROS) and nitric oxide (NO) are important participa
nts in signal transduction that could provide the cellular basis for activi
ty-dependent regulation of neuronal excitability. In young rat cortical bra
in slices and undifferentiated PC12 cells, paired application of depolariza
tion/agonist stimulation and oxidation induces long-lasting potentiation of
subsequent Ca2+ signaling that is reversed by hypoxia. This potentiation c
ritically depends on NO production and involves cellular ROS utilization. T
he ability to develop the Ca2+ signal potentiation is regulated by the deve
lopmental stage of nerve tissue, decreasing markedly in adult rat cortical
neurons and differentiated PC12 cells.