Propofol can Protect Against the Impairment of Learning-memory Induced by Electroconvulsive Shock via Tau Protein Hyperphosphorylation in Depressed Rats

Objective To explore the possible neurophysiologic mechanisms of propofol and N-methyl-Daspartate(NMDA) receptor antagonist against learning-memory impairment of depressed rats without olfactory bulbs. Methods Models of depressed rats without olfactory bulbs were established. For the factorial design in analysis of variance, two intervention factors were included: electroconvulsive shock groups(with and without a course of electroconvulsive shock) and drug intervention groups [intraperotoneal(ip) injection of saline, NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed rats without olfactory bulbs were randomly divided into 6 experimental groups(n=10 per group): ip injection of 5 ml saline; ip injection of 5 ml of 10 mg/kg MK-801; ip injection of 5 ml of 10 mg/kg MK-801 and a course of electroconvulsive shock; ip injection of 5 ml of 200 mg/kg propofol; ip injection of 5 ml of 200 mg/kg propofol and a course of electroconvulsive shock; and ip injection of 5 ml saline and a course of electroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water maze test. The content of glutamic acid in the hippocampus was detected by high-performance liquid chromatography. The expressions of p-AT8Ser202 in the hippocampus were determined by Western blot analysis. Results Propofol, MK-801 or electroconvulsive shock alone induced learning-memory impairment in depressed rats, as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up-regulated by electroconvulsive shock and down-regulated by propofol, but MK-801 had no significant effect on glutamic acid content. Levels ofphosphorylated Tau protein p-AT8Ser202 in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8Ser202 levels induced by electroconvulsive shock. Conclusion Electroconvulsive shock might reduce learning-memory impairment caused by protein Tau hyperphosphorylation in depressed rats by down-regulating glutamate content.

Learning-Memory Function and Swimming Capability of Rat and Ergonomic Evaluation Under Hypoxic Condition

Effects of hypoxia on learning-memory function and swimming capability of rat were studied and the ergonomics under hypoxic condition was also evaluated from the biological point of view.Three modes of hypoxia were designed and plots of oxygen concentration versus time for each group in hypoxic environment were produced.Results showed that the effects of hypoxia on learning-memory function and swimming capability were related with the time and strength of hypoxia.It had nothing to do with the individual difference of rat models.10% O2 long-term intermittent anamorphosis hypoxia could improve the swimming capability of rat model significantly.Stimulating with proper level of hypoxia,carbon dioxide could improve ergonomics in airtight hypoxia environment.Under hypoxia condition,from the ergonomic point of view,6% O2 is the important threshold and might belong in critical region.

Protective Effects and Mechanism of Puerarin on Learning-Memory Disorder after Global Cerebral Ischemia-Reperfusion Injury in Rats

Objective:To observe the effect of puerarin on the learning-memory disorder after global cerebral ischemia-reperfusion injury in rats,and to explore its mechanism of action.Methods:The global cerebral ischemia-reperfusion injury model was established using the modified Pulsinelli four-vessel occlusion in Sprague-Dawley rats.Rats were intraperitoneally injected with puerarin(100 mg/kg) 1 h before ischemia and once every 6 h afterwards.The learning-memory ability was evaluated by the passive avoidance test.Th...

Influence of Samarium on Learning and Memory Function of Rats

Sixty-four Spraque-Dawley(SD)big rats with weaning weight of (195±15) g were randomly divided into 4 groups with 8 males and 8 females each group. One group drunk with de-ionized water served as control and was also used for analysis of the background. The other three groups rats were raised by de-ionized water containing low, middle and high concentrations of Sm for four months, then learning and memory tests were carried out in Y-electric maze. Compared with the control rats, the learning and memory of rats in low and middle groups shows a deterioration trend, exhibiting the function degradation of rats' brain. It may results from the rare earth elements through blood-brain barrier affecting the normal physiological functions of rats' brain. In addition, the activity of superoxide dismutase (SOD) in rats' brain decreases, while the content of malondialdehyde (MDA) concentration increases. The decreased SOD activity and the increased MDA mean the degeneration the ability of anti-oxidation in rats' brain, which are accordance with the degradation of learning and memory function of rats in low and middle Sm groups.