RESUMEN
Objective To investigate the effect of fast-aging on the excitability of hippocampus CA1 neurons in mouse and the possible interaction between fast-aging and hippocampus. Methods Using brain slice and extracellular recording technique to record the firing of hippocampus CA1 neurons in fast-aging(SA M-P/8) and normal control mice, after preprocessing, neural firing train were obtained. Using neural firing rate and inter-spike-inter to investigate interaction between fast-aging and hippocampal neural firing. Results The neural firing rate of hippocampus CA1 neurons in fast-aging mice is (1.052±0.364) Hz(n=14), while the neural firing ratein normal control mice is (4.416±1.306) Hz(n=22). In fast-aging mice, 80.5% inter spike intervel(ISI) is longerthan 1sec, but in normal control mice, 95.6% ISI is shorter than 0.5sec. Conclusion The decreased firing rate of hippocampus CA1 and longer ISI observed in the fast-aging mice indicates that fast-aging significantly inhibit hippocampal CA1 neurons excitability.
RESUMEN
To investigate the effects of ischemia-reperfusion on the levels of nitric oxide and nitric oxide synthase isoforms (nNOS and iNOS), rat organotypic hippocampus slice were cultured in vitro and subjected to ischemia by oxygen glucose deprivation (OGD) for 30 min and then placed in the normal culture condition. The ischemia-reperfusion produced a time-dependent increase in nitrite levels in the culture medium. Reverse transcriptional-polymerase chain reaction showed augmented levels of mRNA for both nNOS and iNOS when compared with control at 12 h and remained increase at 36 h after OGD (P＜0.05). The protein levels of both nitric oxide synthase isoforms increased significantly as determined by Western Blot. OGD also caused neurotoxicity in this model as revealed by the elevated lactate dehydrogenase (LDH) efflux into the incubation solution. The results suggest that organotypic hippocampus slice is a useful model in studying ischemia-reperfusion brain injury. NO and NOS may play a critical role in the ischemia-reperfusion brain damage in vitro.