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

Citation
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
Citations number
45
Categorie Soggetti
Physiology
Journal title
ACTA PHYSIOLOGICA SCANDINAVICA
ISSN journal
00016772 → ACNP
Volume
169
Issue
1
Year of publication
2000
Pages
79 - 85
Database
ISI
SICI code
0001-6772(200005)169:1<79:DINOPA>2.0.ZU;2-3
Abstract
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.