Enhancement of sodium taurocholate to the absorption of cefquinome

The objective of the research was to detect the enhancement effect of sodium taurocholate on the absorption of cefquinome both in Caco-2 cells and rats. The absorption efficiency of cefquinome was determined by high performance liquid chromatography and calculated with apparent permeability coefficients [Papp] after Caco-2 cell monolayers treated odium taurocholate [2 mmol/L] and cefquinome. The results showed that the absorption of cefquinome in Caco-2 cell monolayers was significantly increased with the sodium taurocholate [2mmol/L]. Similar results were also detected in the rats orally administrated with 1 mL PBS of cefquinome [20mg/mL] containing different concentration of sodium taurocholate [5 mmol/L, 10mmol/L and 20mmol/L] respectively. Compared with control group, sodium taurocholate at 10 and 20 mmol/L increased the absorption of cefquinome in rats from 0.26 +/- 0.04micro g/mL to 0.57 +/- 0.03micro g/mL, 0.78 +/- 0.07micro g/mL respectively. These results indicated that sodium taurocholate could increase the intestinal permeability in a concentration-dependent mode, which will be useful for clinical treatment

Involvement of stress-induced hippocampal synaptic potentiation in the novelty acquisition / 生理学报

To study the influence of behavioral stress on hippocampal spatial learning and memory, we used the freely moving rats that had undergone chronic implantation of a recording electrode in the hippocampus CA1 region and a bipolar stimulating electrode in the ipsilateral Schaffer collateral-commissural pathway. The field excitatory postsynaptic potentials (fEPSPs) were recorded in the absence of exogenous induction of high-frequency stimulation (HFS) or low-frequency stimulation (LFS) and reflected the effect of stress on the hippocampal spatial learning. And we also investigated the change of hippocampal synaptic plasticity when rats were re-exposed to the same environment at 24 h after novelty acquisition. We found that exploration of a novel environment induced the hippocampal synaptic depression in the rats with stress-adaption, whereas exposure to the novel environment induced the hippocampal synaptic potentiation in the behavioral stress rats. Furthermore, re-exposure to the same environment no longer elicited the hippocampal synaptic potentiation or depression at 24 h after the first novel acquisition in the behavioral stress rats. These results demonstrate that behavioral stress induces the hippocampal synaptic potentiation under novelty acquisition and further damages the hippocampal spatial learning and memory. However, the stress can be adapted by re-exposure to the novelty and thus does not further damage the hippocampal spatial learning and memory.

Dopamine-dependent long-term depression in hippocampus of rat induced by exposure to spatial novelty / 生理学报

To study the role of long-term depression (LTD) in the mechanisms of learning and memory in hippocampus of rat, recordings were taken from freely moving animals that had undergone chronic implantation of a recording electrode in the hippocampus CA1 region and a bipolar stimulating electrode in the ipsilateral Schaffer collateral-commissural pathway. The recording electrode was inserted 3.8 mm posterior to bregma and 2.8 mm right of the midline, and the stimulating electrode was inserted 4.8 mm posterior to bregma and 3.8 mm right of the midline via holes drilled through the skull. The entire assembly was connected with a rubber socket on the animal's head and then stabilized with dental cement. The correct placement of the electrodes into the hippocampal CA1 area was confirmed via electrophysiological criteria and postmortem histological analysis. After 2 weeks of surgery recovery, the rats were placed in the familiar recording chamber for 3 days. The field excitatory postsynaptic potentials (fEPSPs) were evoked by stimulating with a square wave constant current pulse of 0.2 ms duration, at a frequency of 0.033 Hz and at a stimulation intensity adjusted to given an fEPSP amplitude of 50% of the maximum, and the baseline of fEPSPs were recorded for 3 days in the familiar recording environment at the same time each day. A novelty environment that was made of clear Perspex (40 cm x 40 cm x 40 cm) was prepared and we examined whether exposure to a novelty spatial environment facilitated the expression of activity-dependent persistent decrease in synaptic transmission (namely LTD) at CA1 synapses in the rat hippocampus. The results showed that brief exposure to a novelty environment for 10 min facilitated the expression of LTD in the hippocampal CA1 area under no other exogenous high- or low-frequency stimulation protocol. This facilitatory effect was dependent on the activation of D1/D5 receptors: the D1/D5 receptors antagonist SCH23390 prevented the decrease of synaptic transmission in the hippocampus during the novelty exploration. These data provided important evidence that LTD may underlie certain forms of learning and memory and that dopamine participates in the synaptic plasticity in the process of hippocampal spatial information storage.