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.

Five percent CO_(2) inhalation alleviates hippocampal glutamate and water homeostasis disturbance,neuronal damage,and learning-memory impairment in sleep-deprived rats

Background:Sleep deprivation causes hippocampal injury,manifesting as neuronal damage and learning-memory impairment.These negative effects may be associated with disturbance of hippocampal glutamate and water homeostasis,which induces excessive neuronal excitability.Five percent CO_(2) inhalation has been shown to suppress neuronal excitability.Here,we aimed to investigate whether 5%CO_(2) inhalation facilitates the recovery of hippocampal glutamate and water homeostasis,neuron morphology,and learning-memory ability in sleep-deprived rats.Methods:Thirty-six Sprague-Dawley female rats were randomly divided into three groups including normal sleep(Group 1,NS,n=12),sleep deprivation followed by sleep recovery(Group 2,SD+SR,n=12),sleep deprivation followed by sleep recovery and 5%CO_(2) inhalation(Group 3,SD+SR+CO_(2),n=12)by random number table.Each group was divided into two subgroups(n=6 each subgroup)for different experiments randomly by random number table.Results:We found that 5%CO_(2) inhalation facilitated the recovery of hippocampal glutamate concentration(7.549±0.310,8.716±0.463,and 7.493±0.281 mmol/L at Days 1,3,and 5 in Group 3,F 2,15=22.06,p<0.0001)and hippocampal apparent diffusion coefficient mean value(8.210±0.274,7.685±0.171,8.265±0.269 at Days 1,3,and 5 in Group 3,F 2,15=10.45,p=0.0014),enhanced expression level of astrocyte-specific membrane protein glutamate transporter-1,promoted the polarized distribution of aquaporin 4,reduced hippocampal neuronal damage and improved learning-memory ability in sleep-deprived rats.Conclusion:This study showed that 5%CO_(2) inhalation can serve as a novel strategy for alleviating sleep deprivation-induced hippocampal injury.

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...

Protective effects of edaravone on diffuse brain njury in rats

BACKGROUND：Edaravone can alleviate brain injury and improve neurological functions and symptoms. This study aimed to investigate the effect of edaravone on the p38Mitogen-activated protein kinases/Caspase-3 （p38MAPK/Caspase-3） pathway after diffuse brain injury （DBI） in rats. METHODS： DBI models were established according to the description of Marmarou＇s method. A total of 250 rats were divided （random number） into four groups： control group （CG, n=45）, model group （MG, n=77）, low-dose edaravone group （n=67, dosage 5 mg/kg） and high-dose edaravone group （n=61, dosage 10 mg/kg）. After 1,6, 24, 48, and 72 hours after injury, brain tissues were collected. The changes of neuron morphous in the hippocampal region were observed through Nissl staining. The expression levels of phosphorylated p38MAPK and caspase-3 were detected by immunohistochemistry and Western blotting respectively. Learning and memory function were tested with Morris water maze from the 3rd to 7th day after injury. RESULTS： Some neurons had histopathologic changes of necrosis and apoptosis in the model group compared with the control group. The phosphorylated p38MAPK expressions increased at 1,6, 4, and 48 hours （P〈0.05）, but no significant difference was observed at 72 hours （0.54±0.19 vs. 0.40±0.14, P〉0.05）. Caspase-3 expressions increased at 6, 24, 48, and 72 hours respectively （P〈0.05）, but there was no significant difference at 1 hour （0.59±0.29 vs. 0.40±0.17, P〉0.05）. From the 3rd to 6th day during the Morris water maze test, the latency to find the platform was significantly prolonged （P〈0.05） and times of rats crossing the platform was decreased on the 7th day （2.28±1.18 vs. 8.20±1.52, P〈0.05）. The phosphorylated p38MAPK expressions decreased at 6, 24 and 48 hours respectively in the low dose edaravone group compared with the model group （P〈0.05）, whereas no significant difference was seen at 1 hour （1.66±0.80 vs. 1.85±0.86, P〉0.05）. Caspase-3 expression decreased at 6, 24, 48, and 72 hours （P〈0.05）. The latency to find the platform was significantly shortened （P〈0.05）, and times of rats crossing the platform increased （4.17±1.15 vs. 2.28±1.18, P〈0.05）. The above mentioned parameters changed more significantly in the high-dose edaravone group than in the low-dose edaravone group. CONCLUSION：Edaravone can alleviate brain tissue damage after DBI, inhibit p38MAP signal activation after early injury, reduce the expression of caspase-3, and promote the recovery of neurological function in the late period.

Influence of Samarium on Learning and Memory Function of Rats

Sixty-four Spraque-Dawley (SD) big rats with weaning weight of (195 qqqqqq 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 rals' brain tie-creases , 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.