Changes of RARα and synaptic plasticity signaling pathway related gene expressions in hippocampus of young rats after morris water maze

2010 ◽  
Vol 34 (8) ◽  
pp. S26-S26
Author(s):  
Xuan Zhang ◽  
Ting‑yu Li ◽  
Ke Chen ◽  
Jie Chen ◽  
You‑xue Liu ◽  
...  
2021 ◽  
pp. 096032712110085
Author(s):  
L Wu ◽  
Y Hu ◽  
L Jiang ◽  
N Liang ◽  
P Liu ◽  
...  

Some traditional Chinese decoctions, such as Zhuyu Annao, exert favorable therapeutic effects on acute cerebral hemorrhage, hemorrhagic stroke, and other neurological diseases, but the underlying mechanism remains unclear. This study aimed to determine whether Zhuyu Annao decoction (ZYAND) protects the injured brain by promoting angiogenesis following intracerebral hemorrhage (ICH) and elucidate its specific mechanism. The effect of ZYAND on the nervous system of mice after ICH was explored through behavioral experiments, such as the Morris water maze and Rotarod tests, and its effects on oxidative stress were explored by detecting several oxidative stress markers, including malondialdehyde, nitric oxide, glutathione peroxidase, and superoxide dismutase. Real-time quantitative RT-PCR and WB were used to detect the effects of ZYAND on the levels of prolyl hydroxylase domain 3 (PHD3), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF) in the brain tissues of mice. The effect of ZYAND on the NF-κB signaling pathway was detected using a luciferase reporter gene. A human umbilical cord vascular endothelial cell angiogenesis experiment was performed to determine whether ZYAND promotes angiogenesis. The Morris water maze test and other behavioral experiments verified that ZYAND improved the neurobehavior of mice after ICH. ZYAND activated the PHD3/HIF-1α signaling pathway, inhibiting the oxidative damage caused by ICH. In angiogenesis experiments, it was found that ZYAND promoted VEGF-induced angiogenesis by upregulating the expression of HIF-1α, and NF-κB signaling regulated the expression of HIF-1α by inhibiting PHD3. ZYAND exerts a reparative effect on brain tissue damaged after ICH through the NF-κB/ PHD3/HIF-1α/VEGF signaling axis.


2019 ◽  
Vol 9 (9) ◽  
pp. 236 ◽  
Author(s):  
Xue Li ◽  
Lu Wang ◽  
Shuling Zhang ◽  
Xiang Hu ◽  
Huijun Yang ◽  
...  

This study was designed to investigate beneficial effects of swimming exercise training on learning/memory, synaptic plasticity and CREB (cAMP response element binding protein) expression in hippocampus in a rat model of d-galactose-induced aging (DGA). Eighty adult male rats were randomly divided into four groups: Saline Control (group C), DGA (group A), Swimming exercise before DGA (group S1), and Swimming during DGA (group S2). These four groups of animals were further divided into Morris water maze training group (M subgroup) and sedentary control group (N subgroup). Spatial learning/memory was tested using Morris water maze training. The number and density of synaptophysin (Syp) and metabotropic glutamate receptor 1 (mGluR1) in hippocampal dentate gyrus area, CREB mRNA and protein expression and DNA methylation levels were determined respectively with immunohistochemistry, western blot, real-time PCR, and MassArray methylation detection platform. We found that compared with group C, DGA rats showed aging-like poor health and weight loss as well as hippocampal neurodegenerative characteristics. Exercise training led to a time-dependent decrease in average escape latency and improved spatial memory. Exercise training group (S2M) had significantly increased swim distance as compared with controls. These functional improvements in S2M group were associated with higher Syp and mGluR1 values in hippocampus (p < 0.01) as well as higher levels of hippocampal CREB protein/mRNA expression and gene methylation. In conclusion, swimming exercise training selectively during drug-induced aging process protected hippocampal neurons against DGA-elicited degenerative changes and in turn maintained neuronal synaptic plasticity and learning/memory function, possibly through upregulation of hippocampal CREB protein/mRNA and reduction of DGA-induced methylation of CREB.


2016 ◽  
Vol 39 (3) ◽  
pp. 1078-1086 ◽  
Author(s):  
Jinhua Wang ◽  
Jie Yuan ◽  
Jingjuan Pang ◽  
Jiang Ma ◽  
Bing Han ◽  
...  

Background/Aims: Chronic stress can lead to cognitive impairment. Senescence-accelerated mouse prone 8 (SAMP8) is a naturally occurring animal model that is useful for investigating the neurological mechanisms of Alzheimer's disease. Here we investigated the impact and mechanisms of chronic stress on cognition in male SAMP8 mice. Methods: Male 6-month- old SAMP8 and SAMR1 (senescence-accelerated mouse resistant 1) mice strains were randomly divided into 4 groups. Mice in the unpredictable chronic mild stress (UCMS) groups were exposed to diverse stressors for 4 weeks. Then, these mice performed Morris water maze (MWM) test to assess the effect of UCMS on learning and memory. To explore the neurological mechanisms of UCMS on cognition in mice, we evaluated changes in the expression of postsynaptic density 95 (PSD95) and synaptophysin (SYN), which are essential proteins for synaptic plasticity. Five mice from each group were randomly chosen for reverse transcription polymerase chain reaction (RT-PCR) and western blotting analysis of SYN and PSD95. Results: The Morris water maze experiment revealed that the cognitive ability of the SAMP8 mice decreased with brain aging, and that chronic stress aggravated this cognitive deficit. In addition, chronic stress decreased the mRNA and protein expression of SYN and PSD95 in the hippocampus of the SAMP8 mice; however, the SAMR1 mice were unaffected. Conclusion: Our results demonstrate that decreased cognition and synaptic plasticity are related to aging. Moreover, we show that chronic stress aggravated this cognitive deficit and decreased SYN and PSD95 expression in the SAMP8 mice. Furthermore, the SAMP8 mice were more vulnerable to the detrimental effects of chronic stress on cognition than the SAMR1 mice. Our results suggest that the neurological mechanisms of chronic stress on cognition might be associated with a decrease in hippocampal SYN and PSD95 expression, which is critical for structural synaptic plasticity.


2020 ◽  
Vol 158 ◽  
pp. 21-29
Author(s):  
Zahra Salimi ◽  
Lotfollah Khajehpour ◽  
Farshad Moradpour ◽  
Ahmad Ali Moazedi ◽  
Ali Pourmotabbed ◽  
...  

2010 ◽  
Vol 469 (3) ◽  
pp. 375-379 ◽  
Author(s):  
Alejandra Arias-Cavieres ◽  
Carlos Rozas ◽  
Miguel Reyes-Parada ◽  
Nelson Barrera ◽  
Floria Pancetti ◽  
...  

2019 ◽  
Vol 16 (2) ◽  
pp. 135-145 ◽  
Author(s):  
Wenjie Hu ◽  
Lin Wen ◽  
Fang Cao ◽  
Yexin Wang

Background: Alzheimer’s Disease (AD) is a chronic progressive neurodegenerative disorder in a central nervous system seen. Objective: We aimed to study the miR-107 in Alzheimer's Disease (AD) pathology through regulating SYK and NF-κB signaling pathway. </P><P> Method: Bioinformatics analysis was performed to screen NF-κB signaling pathway and differentially expressed genes. The target relationship between miR-107 and SYK was verified by dual luciferase assay. QRT-PCR and western blot analysis were used to verify the expression level of miR-107, SYK and NF- κB signaling pathway related proteins of hippocampus primary neurons. BAY61-3606 and BAY11-7082 were purchased for functional examination. Morris water maze tests were performed to access spatial memory of AD mice with SYK and NF-κB signaling pathway inhibition. Fluorescence microscope dyeing experiment investigated the neurons nuclear form and apoptosis. Results: MiR-107 was lowly expressed while SYK was highly expressed in Tg19959 mouse model. Luciferase Assay confirmed the target relationship in miR-107 and SYK. With the inhibition of miR-107, SYK was up-regulated and the increase of p-p65 and the decrease of p-IκB-α suggested that NF-κB signaling pathway was activated in vitro. Morris water maze test indicated that the spatial memory of Tg19959 mice was increased with the treatment. The result of DAPI staining indicated that the inhibition of SYK or NF-κB signaling pathway reduced the apoptosis of Tg19959 mice neuron cell. Conclusion: MiR-107 exerts its effects through suppression of the NF-κB signaling pathway and SYK, the inhibition of SYK and NF-κB signaling pathway can improve spatial memory and suppress cell apoptosis.


Author(s):  
Е.И. Захарова ◽  
З.И. Сторожева ◽  
А.Т. Прошин ◽  
М.Ю. Монаков ◽  
А.М. Дудченко

Цель - исследование холинергической синаптической организации функций обучения и памяти у крыс с разными когнитивными способностями. Методы. Крыс обучали на пространственной обстановочной модели в водном лабиринте Морриса. Через 2-3 сут. после окончания тренировок животных декапитировали, из неокортекса и гиппокампа с помощью центрифугирования выделяли субфракции синаптических мембран и синаптоплазмы легких и тяжелых синаптосом. В синаптических субфракциях определяли активность ключевого фермента холинергических нейронов холинацетилтрансферазы (ХАТ). Сравнивали результаты тестирования (время достижения скрытой платформы) и активность фермента у способных и неспособных к обучению крыс. Результаты. Были выявлены: 1) различия в холинергической организации исследованных функций в процессе обучения у способных и неспособных к обучению крыс, в том числе: положительные корреляции активности ХАТ в синапсах проекционных нейронов неокортекса у способных крыс со временем достижения платформы на промежуточных этапах обучения и в синапсах проекционных нейронов гиппокампа у неспособных крыс на позднем этапе обучения; разнонаправленные корреляции активности ХАТ в синапсах, предположительно, интернейронов гиппокампа (фракция тяжелых синаптосом) у способных и неспособных крыс на начальном и позднем этапах обучения; 2) индивидуальность холинергической организации функций на всех этапах обучения. Выводы. Полученные данные свидетельствуют в пользу представлений о специфике холинергической организации функций пространственного обстановочного обучения у крыс с выраженными и слабыми способностями к обучению, а также избирательной роли холинергических интернейронов гиппокампа на исходном этапе обучения и в консолидации памяти. In order to expand the knowledge about neuronal organization of the cognitive functions required for understanding plastic processes in the brain, we investigated the cholinergic synaptic organization of learning and memory functions in rats with different cognitive abilities. Methods. Rats were trained on a contextual situation model in the Morris water maze. At 2-3 days after the end of training, animals were decapitated, and subfractions of synaptic membranes and synaptoplasm of light and heavy synaptosomes were isolated from the cortex and the hippocampus by centrifugation. In synaptic subfractions, activity of the key enzyme of cholinergic neurons, choline acetyltransferase, was measured. We compared the test results (latent period to reach the hidden platform) and the enzyme activity in capable (lower quartile) and incapable of learning rats (upper quartile). Results. The following was found: 1) differences in the cholinergic organization of studied functions in capable and uncapable of learning rats during training, including: positive correlations of choline acetyltransferase activity in synapses of projection neurons in the cortex of capable rats with latency to reach the platform at intermediate stages of training and in the hippocampus ofincapable rats at late stages of training; multidirectional correlations of choline acetyltransferase activity in synapses of hippocampal, presumably, interneurons (heavy synaptosomes) in capable and incapable rats at early and late stages of training; 2) distinctness of the cholinergic organization of functions at all stages of training. Conclusions. The study demonstrated for the first time a specificity of the cholinergic organization of functions in spatial situational learning of rats with strong and poor learning abilities and a selective role of hippocampal cholinergic interneurons at the initial stage of learning and in memory consolidation.


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