Effect of Aluminum on Long-Term Potentiation and Its Relation to L-arg-No-pathway in Hippocampal CA3 Area of Rats

Experiments were performed on 64 Sprague-Dawley rats under ure-thane anesthesia. Extracellular recording method was used to investigate the effect of aluminum (Al)microinjected into CA3 on long-term potentiation (LTP) in this area. The relationship between the inhibitory effect of Al and L-arginine-NO pathway was also studied. Microinjection of Al (0. 5 mol/L, 1 μl ) into CA3 could block the induction of LTP in CA3. Microinjection of Al (0. 5 mol/L, 1 μl) into CA3 after LTP was induced could also decrease the amplitude of population spike (PS). The inhibitory effect of Al on LTP in CA3 could be enhanced by preinjection of NG-nitro-L-arginine (0. 3 mol/L, 1 μl). Preinjection of L-arginine (0. 3 mol/L, 1 μl) into CA3 could antagonize the inhibitory effect of Al on LTP. These results suggest that Al could block the induction of LTP and decrease the amplitude of PS potentiated in CA3. The effect of Al might be antagonized by L-arginine-NO pathway.

Sedimentary microfacies of the H8 member in the Su14 3D seismic test area

The distribution of sedimentary microfacies in the eighth member of the Shihezi formation（the H8 member） in the Sul4 3D seismic test area was investigated.A Support Vector Machine（SVM） model was introduced for the first time as a way of predicting sandstone thickness in the study area.The model was constructed by analysis and optimization of measured seismic attributes.The distribution of the sedimentary microfacies in the study area was determined from predicted sandstone thickness and an analysis of sedimentary characteristics of the area.The results indicate that sandstone thickness predictions in the study area using an SVM method are good.The distribution of the sedimentary microfacies in the study area has been depicted at a fine scale.

Traumatic brain injury impairs synaptic plasticity in hippocampus in rats

Background Traumatic brain injury （TBI） often causes cognitive deficits and remote symptomatic epilepsy. Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBI may impair the cellular circuit in the hippocampus.Methods Forty male Wistar rats were randomized into control （n=-20） and TBI groups （n=20）. Long-term potentiation, extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.Results TBI resulted in a significantly increased excitability in the dentate gyrus （DG）, but a significantly decreased excitability in the cornu ammonis 1 （CA1） area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area. Conclusions TBl leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.