Deficits in nitric oxide production after tetanic stimulation are related to the reduction of long-term potentiation in Schaffer-CA1 synapses in agedFischer 344 rats
K. Mori et al., Deficits in nitric oxide production after tetanic stimulation are related to the reduction of long-term potentiation in Schaffer-CA1 synapses in agedFischer 344 rats, ACT PHYSL S, 169(1), 2000, pp. 79-85
In the present study, we investigated whether nitric oxide (NO) production
after tetanic stimulation is involved in long-term potentiation (LTP) in Sc
haffer-CA1 synapses in both young adult and aged rats. The changes in both
the population spike amplitude and NO metabolites, nitrite (NO2-) and nitra
te (NO3-), in the CA1 region were simultaneously determined before and afte
r 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 signif
icantly inhibited compared with that in young adult rats. No increase in NO
x 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 reduct
ion of LTP formation in aged rats.