Deficits in nitric oxide production after tetanic stimulation are related to the reduction of long-term potentiation in Schaffer-CA1 synapses in aged Fischer 344 rats.

In the present study, we investigated whether nitric oxide (NO) production after tetanic stimulation is involved in long-term potentiation (LTP) in Schaffer-CA1 synapses in both young adult and aged rats. The changes in both the population spike amplitude and NO metabolites, nitrite (NO2-) and nitrate (NO3-), in the CA1 region were simultaneously determined before and after tetanic stimulation. Increases in NOx (NO2- plus NO3-) levels in the CA1 region were observed after tetanic stimulation in young adult rats as well as increase in the population spike amplitude. In aged rats, LTP was significantly inhibited compared with that in young adult rats. No increase in NOx level after tetanic stimulation was observed in aged rats. These findings directly demonstrated that NO production might be involved in the process of LTP formation in Schaffer-CA1 synapses of the rat hippocampus, and that the deficiency of hippocampal NO production might be responsible for reduction of LTP formation in aged rats.