Lead （Pb） is ubiquitous in the environment, and low-level Pb exposure can cause neurotoxicity and irreversible damage to children＇s cognition, learning and memory ability. Nutritional intervention is an effective m...Lead （Pb） is ubiquitous in the environment, and low-level Pb exposure can cause neurotoxicity and irreversible damage to children＇s cognition, learning and memory ability. Nutritional intervention is an effective method to prevent Pb poisoning. Mul- berry is rich in anthocyanins, possessing protective effects for nerves. This study investigated the neuroprotective effects of mulberry extract （ME） against Pb-induced learning and memory deficits in mice. The results showed that the learning and memory abilities of mice, assessed using the Morris test, improved significantly after treatment with ME at a dose of 100 mg/kg body weight. The level of Pb in the brains of mice in the three ME intervention groups decreased significantly, while NO production and anti-oxidant enzymes were significantly restored. It is suggested that ME inhibits Pb-induced neurotoxicity by reversing Pb-induced alterations in the aspect of neurotoxic effects and improving learning and memory.展开更多
Objective:To investigate the possible mechanism of microRNA-9-5p(miR-9-5p)and Ras homologous gene family A(RHOA)in aluminum-induced cognitive dysfunction in rats.Methods:According to the principle of randomization,48 ...Objective:To investigate the possible mechanism of microRNA-9-5p(miR-9-5p)and Ras homologous gene family A(RHOA)in aluminum-induced cognitive dysfunction in rats.Methods:According to the principle of randomization,48 Wistar rats were randomly divided into four groups(n=12)of blank control,low dose,medium dose and high dose.The blank control group was gavaged daily saline,and the other three dose groups were given daily gavage AlCl3 aqueous solution at three doses of 25 mg/kg,50 mg/kg,and 100 mg/kg to create a rat model of cognitive impairment for three months.The water maze(MWM)positioning navigation experiment was used to record the time t(s),namely,the incubation period,on the platform of rats,and the incubation period of each group was used to determine whether the rats in the infected group had learning and memory impairment.Hematoxylin-eosin(HE)and Nissl stains observed the pathological changes of nerve cells in the hippocampus of the four groups.Western blot detected the protein expression levels of RHOA and cranial neurotrophic factor(BDNF)in fresh rat hippocampal tissues.RT-qPCR detected the mRNA expression of miR-9-5p,RHOA,and BDNF in rat hippocampal tissues.Results:The results of Morris water maze positioning navigation test showed that the incubation period of each group was calculated on the 1st,3rd and 5th days of the experiment,and the motor incubation period of the infected group was higher than that of the control group.The results of HE staining showed that the rat nerve cells in the control group were morphologically intact,the staining was clear,the nucleus was clearly visible,and the edge of the cell membrane was sharp.The rat neurons in the infected group were damaged to varying degrees,the nucleus gradually dissolved,the cytoplasmic staining became deeper,the edges of the cell membrane were blurred and disordered,and the cells were deformed and arranged disordered.The results of Nissl staining showed that the well-stained Nissl body particles were visible in the nerve cells of rats in the control group,and the dissipation of Nissl bodies in the nerve cells of the infected group was reduced,and the staining was shallow.The results of RT-qPCR showed that compared with the control group,the mRNA expression of miR-9-5p and BDNF was decreased in the infected group,and the mRNA expression of RHOA was increased(P<0.05 or P<0.001).The Western blot results showed that compared with the control group,the relative expression of BDNF in the three infected groups was decreased,and the relative expression of RHOA increased(P<0.05).Conclusion:In aluminum-induced cognitive impairment,miR-9-5p is downregulated and RHOA is upregulatd.展开更多
Objective To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. Methods A passive smoking model of pre...Objective To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. Methods A passive smoking model of pregnant mice was established. Learning and memory ability was evaluated by the water maze test and long term potentiation （LTP）. Nitric oxide （NO）, content, nitric oxide synthase （NOS）, acetylcholinesteras （Ache） activity in brain, vitamin E concentration, and reactive oxygen species （ROS） in serum were determined. The latency period （the time during which the mice swim from the starting position to the ending position） and errors （the number of mice entering the blind end） in control and antioxidant intervention groups were compared with those in the smoke exposure group after 6 days. Results The latency period as well as errors in the air, control diet, tobacco smoke （TS）, and vitamin E diet groups were decreased significantly as compared with the TS and control diet groups （P〈O.05）. LTP was restrained in the TS and control diet groups. LTP in all the antioxidant diet groups was significantly increased compared with the TS and control diet groups. In addition, NOS and acetylcholinesteras （Ache） activitiy was significantly higher in the TS and control diet groups than in the air and control diet group. NO content was not significantly different among the different groups, and significantly lower in the TS and vitamin E diet groups than in the TS group, control diet group, quercetin diet group, and mixture diet group （P〈0.05）. Vitamin E concentration and ROS activity in serum were correlated with the outcome of water maze and LTP. Conclusion Passive smoking reduces LTP formation by disturbing the hippocampus function of mice, by decreasing NOS （especially vitamin E） partially improve the learning and memory smoke during pregnancy. and Ache activity and increasing NO content. Antioxidants ability of offsprings whose mothers are exposed to tobacco展开更多
In the present study,Fmr1 knockout mice （KO mice） were used as the model for fragile X syndrome.The results of step-through and step-down tests demonstrated that Fmr1 KO mice had shorter latencies and more error cou...In the present study,Fmr1 knockout mice （KO mice） were used as the model for fragile X syndrome.The results of step-through and step-down tests demonstrated that Fmr1 KO mice had shorter latencies and more error counts,indicating a learning and memory disorder.After treatment with 30,60,90,120,or 200 mg/kg lithium chloride,the learning and memory abilities of the Fmr1 KO mice were significantly ameliorated,in particular,the 200 mg/kg lithium chloride treatment had the most significant effect.Western blot analysis showed that lithium chloride significantly enhanced the expression of phosphorylated glycogen synthase kinase 3 beta,an inactive form of glycogen synthase kinase 3 beta,in the cerebral cortex and hippocampus of the Fmr1 KO mice.These results indicated that lithium chloride improved learning and memory in the Fmr1 KO mice,possibly by inhibiting glycogen synthase kinase 3 beta activity.展开更多
Previous studies have shown that chrysophanol protects against learning and memory impairments in lead-exposed adult mice. In the present study, we investigated whether chrysophanol can alleviate learning and memory d...Previous studies have shown that chrysophanol protects against learning and memory impairments in lead-exposed adult mice. In the present study, we investigated whether chrysophanol can alleviate learning and memory dysfunction and hippocampal neuronal injury in lead-exposed neonatal mice. At the end of lactation, chrysophanol（0.1, 1.0, 10.0 mg/kg） was administered to the neonatal mice by intraperitoneal injection for 15 days. Chrysophanol significantly alleviated injury to hippocampal neurons and improved learning and memory abilities in the lead-poisoned neonatal mice. Chrysophanol also significantly decreased lead content in blood, brain, heart, spleen, liver and kidney in the lead-exposed neonatal mice. The levels of malondialdehyde in the brain, liver and kidney were significantly reduced, and superoxide dismutase and glutathione peroxidase activities were significantly increased after chrysophanol treatment. Collectively, these findings indicate that chrysophanol can significantly reduce damage to hippocampal neurons in lead-exposed neonatal mice.展开更多
Objective: To observe the effects of Bushen Huoxue Formula (Formula for reinforcing the kidney and activating blood circulation) on the learning and memory function and the cerebral neurotransmitters in diabetic mice....Objective: To observe the effects of Bushen Huoxue Formula (Formula for reinforcing the kidney and activating blood circulation) on the learning and memory function and the cerebral neurotransmitters in diabetic mice. Methods: Forty ICR mice were randomized into the normal control group, model group, Nimotop group and Chinese medicine group, 10 mice in each group. Tail intravenous injection of alloxan was applied to prepare diabetic model. Four weeks later, intragastric administration of Bushen Huoxue Formula for the Chinese medicine group, Nimotop for the Nimotop group, and isometric distilled water for the other two groups were respectively given for 8 weeks. The changes in the blood sugar level were observed; the learning and memory function was detected by Morris labyrinth test; and the contents of norepinephrine (NE), dopamine (DA), 5-hydroxyltryptamine (5-HT) and 5-hydroxyl indole acetic acid (5-HIAA) in cerebral cortex were determined in mice of all the groups. Results: The blood sugar levels in the diabetic model mice significantly increased as compared with those of the normal control group determined 72 h and 12 weeks later (P<0.05 or P<0.01). Latencies for Morris labyrinth test in the Nimotop group and the Chinese medicine group were significantly shortened as compared with that in the model group (P<0.01). The contents of cortical NE in the Chinese medicine group was significantly higher than that in the model group (P<0.01). Conclusion: Bushen Huoxue Formula can improve the learning and memory function in the diabetic mice, and the mechanism is possibly related with change of the cortical NE content.展开更多
Objective:Virgin coconut oil(VCO)has been used in the management of dementia in Alzheimer’s disease(AD).Therefore,this research investigated the effect of long-term consumption of VCO diet on learning and memory in C...Objective:Virgin coconut oil(VCO)has been used in the management of dementia in Alzheimer’s disease(AD).Therefore,this research investigated the effect of long-term consumption of VCO diet on learning and memory in CD1 mice.Methods:Thirty male CD1 mice(divided into three groups,n=10)were fed with standard rodent chow(control),5%and 20%VCO diets(respectively)for 28 d.The Morris Water Maze(MWM)test was used to test the effect of VCO on visuo-spatial learning and memory,while the Novel Object Recognition Test(NORT)was used to measure short-and long-term recognition memory.Results:Learning performance of mice did not differ in the MWM.During the probe trial,duration in the retention quadrant and annulus crossings were lower(P<0.05)in the 5%and 20%VCO diet groups compared to the control diet group,showing that VCO impaired visuo-spatial memory.During the NORT,mice showed more total approaches in the 20%VCO diet group(P<0.05)compared to control and the 5%VCO diet groups during the short-term memory test.During the long-term memory retention test,the total approaches were also higher in the 20%VCO group compared to control and 5%VCO group(P>0.05).The discrimination index was also lower in the 20%VCO group compared to control and 5%VCO diet groups indicating impaired long-term cognitive memory in mice given 20%VCO diet.Histological examination of brains showed damage within the CA1 pyramidal cell layer of the hippocampus in the 20%VCO diet group,in line with the behavioural observations.Conclusion:Long-term consumption of virgin coconut oil diet impairs memory in mice.展开更多
The learning ability of the Kh.DIC mice, a mutant of the Kunming mice, was studied to analyze its memory development. The mice's brain function was evaluated using a water maze with the amount of monoamines measur...The learning ability of the Kh.DIC mice, a mutant of the Kunming mice, was studied to analyze its memory development. The mice's brain function was evaluated using a water maze with the amount of monoamines measured by fluorospectrophotometry and enzyme activities detected by ultraviolet spectrophotometry. The mice were found to have spacial learning and memory defects at the age of 1 month in both ordinary animals and in special pathogen free (SPF) animals. At the same time, the amount of monoamines and the activities of monoamine oxidase B and dopamine β hydroxylase differed from those of the Kunming mice. The defects might be related to the differences in the monoamine neurotransmitter system. The results suggest that the DIC mice may be useful economic animal models for the study of brain defects.展开更多
Objective To study the co-effect of procyanidins extracted from the lotus seed pod （LSPC） and bilobalide （BIL） on ameliorating scopolamine-induced learning and memory impairment in young mice. Methods Fifty male K...Objective To study the co-effect of procyanidins extracted from the lotus seed pod （LSPC） and bilobalide （BIL） on ameliorating scopolamine-induced learning and memory impairment in young mice. Methods Fifty male Kunming mice with similar learning and memory capabilities were selected by Morris water maze test and were randomized into 5 groups （n=10 in each group）： control group, scopolamine group, L-（LSPC＋BIL） group （50 mg/kg LSPC＋10 mg/kg BIL）, M-（LSPC＋BIL） group （100 mg/kg LSPC＋20 mg/kg BIL）, H-（LSPC＋BIL） group （150 mg/kg LSPC＋30 mg/kg BIL）. Scopolamine model with impaired learning and memory was established by scopolamine treatment （1 mg/kg）, and after 10 min mice were tested. In L-, M-, and H- （LSPC＋BIL） groups, mice were treated with LSPC and BIL ig. for 30 days, while mice in the other 2 groups were treated with normal saline ig. instead. After the 30-day＇s treatment, the co-effect of LSPC and BIL on learning and memory was tested by Morris water maze and the step-down avoidance tests. Results The memory impairment caused by scopolamine in young mice could be ameliorated by co-treatment of LSPC and BIL, as indicated by significantly shorter escape latency and swimming distance in the Morris water maze test, when compared with those in the scopolamine group. In the step-down avoidance test, mice in all the 3 dose groups showed significantly smaller number of errors and longer latency than mice in the scopolamine group did. Conclusion Co-treatment of LSPE and BIL can ameliorate scopolamine-induced learning and memory impairment in young mice.展开更多
5×FAD转基因小鼠(transgenic mice with five familial Alzheimer’s disease)是携带5个家族性基因突变的APP/PS1转基因小鼠,其中与β-淀粉样蛋白前体(amyloid precursor protein,APP)相关的突变为K670N/M671L(Swedish)、1716V(Flo...5×FAD转基因小鼠(transgenic mice with five familial Alzheimer’s disease)是携带5个家族性基因突变的APP/PS1转基因小鼠,其中与β-淀粉样蛋白前体(amyloid precursor protein,APP)相关的突变为K670N/M671L(Swedish)、1716V(Florida)和V7171(London),与早老素-1(presenilin 1,PS1)相关的突变为MI46L和L286V。5×FAD小鼠在1.5月龄时脑内已有大量的β-淀粉样蛋白(β-amyloid,Aβ),2月龄时开始出现神经炎性斑(neuritic plaque,NP)。5×FAD小鼠的病理表型包括淀粉样斑块聚集、神经元丢失、神经胶质细胞增生和记忆功能障碍等。5×FAD小鼠的生物学特性可能涉及脑内Aβ斑块的形成变化、Tau蛋白过度磷酸化、突触功能障碍、神经炎症反应、线粒体功能障碍、血脑屏障损伤、神经元损伤、内质网应激和眼部病变等。作为阿尔茨海默病的经典动物模型,5×FAD转基因小鼠在早期即可模拟AD患者晚期的神经病理过程及行为学表现,被广泛应用于AD发病机制研究和AD新药开发。本文对5×FAD转基因小鼠模型的模型构建、生物学背景、生物学特性及AD防治药物的研发应用进行总结,以期为5×FAD转基因小鼠在AD研究中的应用提供参考与借鉴作用。展开更多
This study concerns the effects of microwave on health because they pervade diverse fields of our lives. The brain has been recognized as one of the organs that is most vulnerable to microwave radiation. Therefore, in...This study concerns the effects of microwave on health because they pervade diverse fields of our lives. The brain has been recognized as one of the organs that is most vulnerable to microwave radiation. Therefore, in this article, we reviewed recent studies that have explored the effects of microwave radiation on the brain, especially the hippocampus, including analyses of epidemiology, morphology, electroencephalograms, learning and memory abilities and the mechanisms underlying brain dysfunction. However, the problem with these studies is that different parameters, such as the frequency, modulation, and power density of the radiation and the irradiation time, were used to evaluate microwave radiation between studies. As a result, the existing data exhibit poor reproducibility and comparability. To determine the specific dose-effect relationship between microwave radiation and its biological effects, more intensive studies must be performed.展开更多
This study examined the impacts of intrauterine murine cytomegalovirus（MCMV） infection on the long-term learning and memory of offspring.Sexually matured male and female BALB/C mice without MCMV infection were ident...This study examined the impacts of intrauterine murine cytomegalovirus（MCMV） infection on the long-term learning and memory of offspring.Sexually matured male and female BALB/C mice without MCMV infection were identified by ELISA and then mated.Seventy pregnant mice were randomly divided into the virus group（n=40） and the control group（n=30）,in which the pregnant mice were subjected to placenta inoculation of MCMV suspension（1 μL,1×106 PFU） or the same amount of cell culture medium,respectively,at gestational age of 12.5 days.Some pregnant mice [virus group（n=20）,control group（n=15）] were sacrificed by cervical dislocation at gestational age of 18.5 days,and the head circumference and brain weight of the mouse fetuses were measured,and the MCMV infection in their brain tissues was detected by PCR.The other pregnant mice [virus group（n=20）,control group（n=15）] delivered naturally,and the learning and memory capability of the offspring at 70-day-old was analyzed by Morris water maze test.The results showed that 28.57% mouse fetuses in the virus group developed viral infection in the brain.Their head circumference and brain weight were significantly reduced as compared with those in the control group（P0.01）.The Morris water maze test revealed that the mouse offspring in the control group found the platform with straight-line trajectories after training.In contrast,the counterparts in the virus group intended to enter the central area,but looked for the platform with a circular trajectory.And the infected mice exhibited prolonged swimming distance and swimming latency（P0.01）.It was concluded that：（1） placenta inoculation of MCMV can cause fetal brain infection and intrauterine development retardation;（2） the offspring of MCMV placenta inoculation mice showed a long-term decline in learning and memory capability.展开更多
Regular exercise has been shown to reduce the risk of Alzheimer’s disease(AD).Our previous study showed that the protein aquaporin 4(AQP4),which is specifically expressed on the paravascular processes of astrocytes,i...Regular exercise has been shown to reduce the risk of Alzheimer’s disease(AD).Our previous study showed that the protein aquaporin 4(AQP4),which is specifically expressed on the paravascular processes of astrocytes,is necessary for glymphatic clearance of extracellular amyloid beta(Aβ)from the brain,which can delay the progression of Alzheimer’s disease.However,it is not known whether AQP4-regulated glymphatic clearance of extracellular Aβis involved in beneficial effects of exercise in AD patients.Our results showed that after 2 months of voluntary wheel exercise,APP/PS1 mice that were 3 months old at the start of the intervention exhibited a decrease in Aβburden,glial activation,perivascular AQP4 mislocalization,impaired glymphatic transport,synapse protein loss,and learning and memory defects compared with mice not subjected to the exercise intervention.In contrast,APP/PS1 mice that were 7 months old at the start of the intervention exhibited impaired AQP4 polarity and reduced glymphatic clearance of extracellular Aβ,and the above-mentioned impairments were not alleviated after the 2-month exercise intervention.Compared with age-matched APP/PS1 mice,AQP4 knockout APP/PS1 mice had more serious defects in glymphatic function,Aβplaque deposition,and cognitive impairment,which could not be alleviated after the exercise intervention.These findings suggest that AQP4-dependent glymphatic transport is the neurobiological basis for the beneficial effects of voluntary exercises that protect against the onset of AD.展开更多
Background: To explore the influence of age-related changes in learning and memory capacity of SAMP10, an Alzheimer's disease (AD) model mice, and provide theoretical foundation for the selection of month age in r...Background: To explore the influence of age-related changes in learning and memory capacity of SAMP10, an Alzheimer's disease (AD) model mice, and provide theoretical foundation for the selection of month age in related experiment. Methods: SAMP10 female mice with the age of 3, 6 and 9 months were used as the objects of experiment, while the age-matched female SAMR1 were used as the controls, with 12 in each group. The learning memory capacity of mice at different age was detected through Morris water maze and step-down passive avoidance test;meanwhile, the acetylcholine, acetylcholinesterase, choline acetyltransferase, and M-cholinergic receptor binding capacity levels were determined to detect the cholinergic system damage degree in mice with different month age. In addition, the contents of monoamine neurotransmitters such as dopamine, 3,4-dihydroxyphenyl acetic acid, homovanillic acid, norepinephrine and 5-HT, as well as those of amino acid transmitters such as glutamic acid, glutamine, aspartic acid,γ-aminobutyric acid, taurine and glycine in the brain cortex were detected by high performance liquid chromatography-electrochemical deposition. Besides, changes in hippocampal neurons were observed through Nissl staining, and the changes of Aβ in hippocampal CA1 and CA2 regions of SAMP10 were also detected by immunohistochemistry so as to explore the effects of age on the memory capacity of SAMP10. Results: It was discovered in the behavior test and AD-related index tests that: there was no significant difference between the age-matched SAMR1 and the SAMP10 at the age of 3 and 6 months. But the 9-months-old mice suffered remarkable senescence characteristics, including obviously declined learning memory capacity;down-regulated neurotransmitter levels, enzyme activities and amino acid expression;reduced hippocampal neuron number;and increased deposition of hippocampal Aβ protein. Conclusion: It is discovered in this study through behavior tests and AD-related indexs detection that, the learning memory capacity of SAMP10 shows age-dependence, which is gradually decreased with the increase of age, and the 9-months-old mice have developed marked memory impairment and senescence characteristics. SAMP10 is the recognized AD model, the appropriate month age for preventive medication is about 7 months, while that for therapeutic medication is 8-9 months.展开更多
基金supported by the National Natural Science Foundation of China(No.31371733)
文摘Lead （Pb） is ubiquitous in the environment, and low-level Pb exposure can cause neurotoxicity and irreversible damage to children＇s cognition, learning and memory ability. Nutritional intervention is an effective method to prevent Pb poisoning. Mul- berry is rich in anthocyanins, possessing protective effects for nerves. This study investigated the neuroprotective effects of mulberry extract （ME） against Pb-induced learning and memory deficits in mice. The results showed that the learning and memory abilities of mice, assessed using the Morris test, improved significantly after treatment with ME at a dose of 100 mg/kg body weight. The level of Pb in the brains of mice in the three ME intervention groups decreased significantly, while NO production and anti-oxidant enzymes were significantly restored. It is suggested that ME inhibits Pb-induced neurotoxicity by reversing Pb-induced alterations in the aspect of neurotoxic effects and improving learning and memory.
基金National Natural Science Foundation Project of China(No.31560294)Guangxi Degree and Postgraduate Education Reform Project in 2021(No.JGY2021208)。
文摘Objective:To investigate the possible mechanism of microRNA-9-5p(miR-9-5p)and Ras homologous gene family A(RHOA)in aluminum-induced cognitive dysfunction in rats.Methods:According to the principle of randomization,48 Wistar rats were randomly divided into four groups(n=12)of blank control,low dose,medium dose and high dose.The blank control group was gavaged daily saline,and the other three dose groups were given daily gavage AlCl3 aqueous solution at three doses of 25 mg/kg,50 mg/kg,and 100 mg/kg to create a rat model of cognitive impairment for three months.The water maze(MWM)positioning navigation experiment was used to record the time t(s),namely,the incubation period,on the platform of rats,and the incubation period of each group was used to determine whether the rats in the infected group had learning and memory impairment.Hematoxylin-eosin(HE)and Nissl stains observed the pathological changes of nerve cells in the hippocampus of the four groups.Western blot detected the protein expression levels of RHOA and cranial neurotrophic factor(BDNF)in fresh rat hippocampal tissues.RT-qPCR detected the mRNA expression of miR-9-5p,RHOA,and BDNF in rat hippocampal tissues.Results:The results of Morris water maze positioning navigation test showed that the incubation period of each group was calculated on the 1st,3rd and 5th days of the experiment,and the motor incubation period of the infected group was higher than that of the control group.The results of HE staining showed that the rat nerve cells in the control group were morphologically intact,the staining was clear,the nucleus was clearly visible,and the edge of the cell membrane was sharp.The rat neurons in the infected group were damaged to varying degrees,the nucleus gradually dissolved,the cytoplasmic staining became deeper,the edges of the cell membrane were blurred and disordered,and the cells were deformed and arranged disordered.The results of Nissl staining showed that the well-stained Nissl body particles were visible in the nerve cells of rats in the control group,and the dissipation of Nissl bodies in the nerve cells of the infected group was reduced,and the staining was shallow.The results of RT-qPCR showed that compared with the control group,the mRNA expression of miR-9-5p and BDNF was decreased in the infected group,and the mRNA expression of RHOA was increased(P<0.05 or P<0.001).The Western blot results showed that compared with the control group,the relative expression of BDNF in the three infected groups was decreased,and the relative expression of RHOA increased(P<0.05).Conclusion:In aluminum-induced cognitive impairment,miR-9-5p is downregulated and RHOA is upregulatd.
文摘Objective To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. Methods A passive smoking model of pregnant mice was established. Learning and memory ability was evaluated by the water maze test and long term potentiation （LTP）. Nitric oxide （NO）, content, nitric oxide synthase （NOS）, acetylcholinesteras （Ache） activity in brain, vitamin E concentration, and reactive oxygen species （ROS） in serum were determined. The latency period （the time during which the mice swim from the starting position to the ending position） and errors （the number of mice entering the blind end） in control and antioxidant intervention groups were compared with those in the smoke exposure group after 6 days. Results The latency period as well as errors in the air, control diet, tobacco smoke （TS）, and vitamin E diet groups were decreased significantly as compared with the TS and control diet groups （P〈O.05）. LTP was restrained in the TS and control diet groups. LTP in all the antioxidant diet groups was significantly increased compared with the TS and control diet groups. In addition, NOS and acetylcholinesteras （Ache） activitiy was significantly higher in the TS and control diet groups than in the air and control diet group. NO content was not significantly different among the different groups, and significantly lower in the TS and vitamin E diet groups than in the TS group, control diet group, quercetin diet group, and mixture diet group （P〈0.05）. Vitamin E concentration and ROS activity in serum were correlated with the outcome of water maze and LTP. Conclusion Passive smoking reduces LTP formation by disturbing the hippocampus function of mice, by decreasing NOS （especially vitamin E） partially improve the learning and memory smoke during pregnancy. and Ache activity and increasing NO content. Antioxidants ability of offsprings whose mothers are exposed to tobacco
基金the National Natural Science Foundation of China,No.30870876the Natural Science Foundation of Guangdong Province,No.815101700100005+2 种基金the Science and Technology Program of Guangdong Province,No.2005B60302004,2008B030301371,2009B030801368the Traditional Chinese Medicineand Combination of Traditional Chinese and Western Medicine Program of Guangzhou,No.2008A52the Medical and Health Scientific Research Program of Guangzhou,No.2009-YB-167
文摘In the present study,Fmr1 knockout mice （KO mice） were used as the model for fragile X syndrome.The results of step-through and step-down tests demonstrated that Fmr1 KO mice had shorter latencies and more error counts,indicating a learning and memory disorder.After treatment with 30,60,90,120,or 200 mg/kg lithium chloride,the learning and memory abilities of the Fmr1 KO mice were significantly ameliorated,in particular,the 200 mg/kg lithium chloride treatment had the most significant effect.Western blot analysis showed that lithium chloride significantly enhanced the expression of phosphorylated glycogen synthase kinase 3 beta,an inactive form of glycogen synthase kinase 3 beta,in the cerebral cortex and hippocampus of the Fmr1 KO mice.These results indicated that lithium chloride improved learning and memory in the Fmr1 KO mice,possibly by inhibiting glycogen synthase kinase 3 beta activity.
基金financially supported by the Science and Technology Commission Foundation of Zhangjiakou City,No.1021098Dthe Medical Scientific Research Project of Health Bureau of Hebei Province,No.20100144+2 种基金the Natural Science Foundation of Hebei Province,No.H2012405016the Innovative Talents Project of Hebei North University,No.CXRC1325the Major Projects of Hebei North University,No.ZD201310
文摘Previous studies have shown that chrysophanol protects against learning and memory impairments in lead-exposed adult mice. In the present study, we investigated whether chrysophanol can alleviate learning and memory dysfunction and hippocampal neuronal injury in lead-exposed neonatal mice. At the end of lactation, chrysophanol（0.1, 1.0, 10.0 mg/kg） was administered to the neonatal mice by intraperitoneal injection for 15 days. Chrysophanol significantly alleviated injury to hippocampal neurons and improved learning and memory abilities in the lead-poisoned neonatal mice. Chrysophanol also significantly decreased lead content in blood, brain, heart, spleen, liver and kidney in the lead-exposed neonatal mice. The levels of malondialdehyde in the brain, liver and kidney were significantly reduced, and superoxide dismutase and glutathione peroxidase activities were significantly increased after chrysophanol treatment. Collectively, these findings indicate that chrysophanol can significantly reduce damage to hippocampal neurons in lead-exposed neonatal mice.
基金supported by the Foundation of Peking Union Medical College Hospital, China (XH-020042)
文摘Objective: To observe the effects of Bushen Huoxue Formula (Formula for reinforcing the kidney and activating blood circulation) on the learning and memory function and the cerebral neurotransmitters in diabetic mice. Methods: Forty ICR mice were randomized into the normal control group, model group, Nimotop group and Chinese medicine group, 10 mice in each group. Tail intravenous injection of alloxan was applied to prepare diabetic model. Four weeks later, intragastric administration of Bushen Huoxue Formula for the Chinese medicine group, Nimotop for the Nimotop group, and isometric distilled water for the other two groups were respectively given for 8 weeks. The changes in the blood sugar level were observed; the learning and memory function was detected by Morris labyrinth test; and the contents of norepinephrine (NE), dopamine (DA), 5-hydroxyltryptamine (5-HT) and 5-hydroxyl indole acetic acid (5-HIAA) in cerebral cortex were determined in mice of all the groups. Results: The blood sugar levels in the diabetic model mice significantly increased as compared with those of the normal control group determined 72 h and 12 weeks later (P<0.05 or P<0.01). Latencies for Morris labyrinth test in the Nimotop group and the Chinese medicine group were significantly shortened as compared with that in the model group (P<0.01). The contents of cortical NE in the Chinese medicine group was significantly higher than that in the model group (P<0.01). Conclusion: Bushen Huoxue Formula can improve the learning and memory function in the diabetic mice, and the mechanism is possibly related with change of the cortical NE content.
文摘Objective:Virgin coconut oil(VCO)has been used in the management of dementia in Alzheimer’s disease(AD).Therefore,this research investigated the effect of long-term consumption of VCO diet on learning and memory in CD1 mice.Methods:Thirty male CD1 mice(divided into three groups,n=10)were fed with standard rodent chow(control),5%and 20%VCO diets(respectively)for 28 d.The Morris Water Maze(MWM)test was used to test the effect of VCO on visuo-spatial learning and memory,while the Novel Object Recognition Test(NORT)was used to measure short-and long-term recognition memory.Results:Learning performance of mice did not differ in the MWM.During the probe trial,duration in the retention quadrant and annulus crossings were lower(P<0.05)in the 5%and 20%VCO diet groups compared to the control diet group,showing that VCO impaired visuo-spatial memory.During the NORT,mice showed more total approaches in the 20%VCO diet group(P<0.05)compared to control and the 5%VCO diet groups during the short-term memory test.During the long-term memory retention test,the total approaches were also higher in the 20%VCO group compared to control and 5%VCO group(P>0.05).The discrimination index was also lower in the 20%VCO group compared to control and 5%VCO diet groups indicating impaired long-term cognitive memory in mice given 20%VCO diet.Histological examination of brains showed damage within the CA1 pyramidal cell layer of the hippocampus in the 20%VCO diet group,in line with the behavioural observations.Conclusion:Long-term consumption of virgin coconut oil diet impairs memory in mice.
基金Supported by Beijing Science Foundation(No. 95 4 98180 1)
文摘The learning ability of the Kh.DIC mice, a mutant of the Kunming mice, was studied to analyze its memory development. The mice's brain function was evaluated using a water maze with the amount of monoamines measured by fluorospectrophotometry and enzyme activities detected by ultraviolet spectrophotometry. The mice were found to have spacial learning and memory defects at the age of 1 month in both ordinary animals and in special pathogen free (SPF) animals. At the same time, the amount of monoamines and the activities of monoamine oxidase B and dopamine β hydroxylase differed from those of the Kunming mice. The defects might be related to the differences in the monoamine neurotransmitter system. The results suggest that the DIC mice may be useful economic animal models for the study of brain defects.
基金supported by the National Key Technology R&D Program of China (No.2006BAD27B08 and 2006BAD27B09-4)
文摘Objective To study the co-effect of procyanidins extracted from the lotus seed pod （LSPC） and bilobalide （BIL） on ameliorating scopolamine-induced learning and memory impairment in young mice. Methods Fifty male Kunming mice with similar learning and memory capabilities were selected by Morris water maze test and were randomized into 5 groups （n=10 in each group）： control group, scopolamine group, L-（LSPC＋BIL） group （50 mg/kg LSPC＋10 mg/kg BIL）, M-（LSPC＋BIL） group （100 mg/kg LSPC＋20 mg/kg BIL）, H-（LSPC＋BIL） group （150 mg/kg LSPC＋30 mg/kg BIL）. Scopolamine model with impaired learning and memory was established by scopolamine treatment （1 mg/kg）, and after 10 min mice were tested. In L-, M-, and H- （LSPC＋BIL） groups, mice were treated with LSPC and BIL ig. for 30 days, while mice in the other 2 groups were treated with normal saline ig. instead. After the 30-day＇s treatment, the co-effect of LSPC and BIL on learning and memory was tested by Morris water maze and the step-down avoidance tests. Results The memory impairment caused by scopolamine in young mice could be ameliorated by co-treatment of LSPC and BIL, as indicated by significantly shorter escape latency and swimming distance in the Morris water maze test, when compared with those in the scopolamine group. In the step-down avoidance test, mice in all the 3 dose groups showed significantly smaller number of errors and longer latency than mice in the scopolamine group did. Conclusion Co-treatment of LSPE and BIL can ameliorate scopolamine-induced learning and memory impairment in young mice.
基金supported by the National Natural Science Foundation of China(61571455).
文摘This study concerns the effects of microwave on health because they pervade diverse fields of our lives. The brain has been recognized as one of the organs that is most vulnerable to microwave radiation. Therefore, in this article, we reviewed recent studies that have explored the effects of microwave radiation on the brain, especially the hippocampus, including analyses of epidemiology, morphology, electroencephalograms, learning and memory abilities and the mechanisms underlying brain dysfunction. However, the problem with these studies is that different parameters, such as the frequency, modulation, and power density of the radiation and the irradiation time, were used to evaluate microwave radiation between studies. As a result, the existing data exhibit poor reproducibility and comparability. To determine the specific dose-effect relationship between microwave radiation and its biological effects, more intensive studies must be performed.
基金supported by grants from National Natural Sciences Foundation of China(No.30371488,No.30672243)Natural Sciences Foundation of Hubei Province of China(No.2009CDB216)
文摘This study examined the impacts of intrauterine murine cytomegalovirus（MCMV） infection on the long-term learning and memory of offspring.Sexually matured male and female BALB/C mice without MCMV infection were identified by ELISA and then mated.Seventy pregnant mice were randomly divided into the virus group（n=40） and the control group（n=30）,in which the pregnant mice were subjected to placenta inoculation of MCMV suspension（1 μL,1×106 PFU） or the same amount of cell culture medium,respectively,at gestational age of 12.5 days.Some pregnant mice [virus group（n=20）,control group（n=15）] were sacrificed by cervical dislocation at gestational age of 18.5 days,and the head circumference and brain weight of the mouse fetuses were measured,and the MCMV infection in their brain tissues was detected by PCR.The other pregnant mice [virus group（n=20）,control group（n=15）] delivered naturally,and the learning and memory capability of the offspring at 70-day-old was analyzed by Morris water maze test.The results showed that 28.57% mouse fetuses in the virus group developed viral infection in the brain.Their head circumference and brain weight were significantly reduced as compared with those in the control group（P0.01）.The Morris water maze test revealed that the mouse offspring in the control group found the platform with straight-line trajectories after training.In contrast,the counterparts in the virus group intended to enter the central area,but looked for the platform with a circular trajectory.And the infected mice exhibited prolonged swimming distance and swimming latency（P0.01）.It was concluded that：（1） placenta inoculation of MCMV can cause fetal brain infection and intrauterine development retardation;（2） the offspring of MCMV placenta inoculation mice showed a long-term decline in learning and memory capability.
基金supported by the National Natural Science Foundation of China,No.81772454(to TW)Natural Science Foundation of Jiangsu,China,No.BK20190655(to QL).
文摘Regular exercise has been shown to reduce the risk of Alzheimer’s disease(AD).Our previous study showed that the protein aquaporin 4(AQP4),which is specifically expressed on the paravascular processes of astrocytes,is necessary for glymphatic clearance of extracellular amyloid beta(Aβ)from the brain,which can delay the progression of Alzheimer’s disease.However,it is not known whether AQP4-regulated glymphatic clearance of extracellular Aβis involved in beneficial effects of exercise in AD patients.Our results showed that after 2 months of voluntary wheel exercise,APP/PS1 mice that were 3 months old at the start of the intervention exhibited a decrease in Aβburden,glial activation,perivascular AQP4 mislocalization,impaired glymphatic transport,synapse protein loss,and learning and memory defects compared with mice not subjected to the exercise intervention.In contrast,APP/PS1 mice that were 7 months old at the start of the intervention exhibited impaired AQP4 polarity and reduced glymphatic clearance of extracellular Aβ,and the above-mentioned impairments were not alleviated after the 2-month exercise intervention.Compared with age-matched APP/PS1 mice,AQP4 knockout APP/PS1 mice had more serious defects in glymphatic function,Aβplaque deposition,and cognitive impairment,which could not be alleviated after the exercise intervention.These findings suggest that AQP4-dependent glymphatic transport is the neurobiological basis for the beneficial effects of voluntary exercises that protect against the onset of AD.
基金the National Natural Science Foundation of China (Grant number:No.81473586,No.81202192).
文摘Background: To explore the influence of age-related changes in learning and memory capacity of SAMP10, an Alzheimer's disease (AD) model mice, and provide theoretical foundation for the selection of month age in related experiment. Methods: SAMP10 female mice with the age of 3, 6 and 9 months were used as the objects of experiment, while the age-matched female SAMR1 were used as the controls, with 12 in each group. The learning memory capacity of mice at different age was detected through Morris water maze and step-down passive avoidance test;meanwhile, the acetylcholine, acetylcholinesterase, choline acetyltransferase, and M-cholinergic receptor binding capacity levels were determined to detect the cholinergic system damage degree in mice with different month age. In addition, the contents of monoamine neurotransmitters such as dopamine, 3,4-dihydroxyphenyl acetic acid, homovanillic acid, norepinephrine and 5-HT, as well as those of amino acid transmitters such as glutamic acid, glutamine, aspartic acid,γ-aminobutyric acid, taurine and glycine in the brain cortex were detected by high performance liquid chromatography-electrochemical deposition. Besides, changes in hippocampal neurons were observed through Nissl staining, and the changes of Aβ in hippocampal CA1 and CA2 regions of SAMP10 were also detected by immunohistochemistry so as to explore the effects of age on the memory capacity of SAMP10. Results: It was discovered in the behavior test and AD-related index tests that: there was no significant difference between the age-matched SAMR1 and the SAMP10 at the age of 3 and 6 months. But the 9-months-old mice suffered remarkable senescence characteristics, including obviously declined learning memory capacity;down-regulated neurotransmitter levels, enzyme activities and amino acid expression;reduced hippocampal neuron number;and increased deposition of hippocampal Aβ protein. Conclusion: It is discovered in this study through behavior tests and AD-related indexs detection that, the learning memory capacity of SAMP10 shows age-dependence, which is gradually decreased with the increase of age, and the 9-months-old mice have developed marked memory impairment and senescence characteristics. SAMP10 is the recognized AD model, the appropriate month age for preventive medication is about 7 months, while that for therapeutic medication is 8-9 months.
