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目的 研究早期母爱剥夺对大鼠成年后的抑郁水平及纹状体前列腺凋亡反应蛋白(par-4)表达的影响,以及甲基化是否参与par-4基因表达的调控.方法 按照随机数字表法,将新生幼鼠按窝分为母爱剥夺组和对照组,每组17只;母爱剥夺组仔鼠在出生后的第1~14天,每天接受6 h母子分离,对照组不接受任何实验处理;13周龄时,采用强迫游泳实验和糖水偏爱实验测定大鼠的抑郁水平,采用实时定量聚合酶链反应检测纹状体par-4及多巴胺受体2(DRD2)信使RNA(mRNA)表达水平,采用亚硫酸盐测序法检测par-4基因启动子区DNA甲基化水平.结果 母爱剥夺组大鼠漂浮时间[(152.80±74.21)s]较对照组[(63.80±80.55)s]延长,糖水偏爱率(0.45±0.23)较对照组(0.69±0.25)降低,差异均有统计学意义(t=2.79,P<0.05;t=-2.57,P<0.05);母爱剥夺组大鼠纹状体内par-4(0.02±0.02)及DRD2 mRNA表达量(0.11±0.09)分别为对照组[(0.04±0.02)、(0.32±0.21)]的0.53倍和0.31倍;母爱剥夺组大鼠par-4基因启动子区DNA甲基化水平与对照组相比差异无统计学意义(t=-0.748,P>0.05).结论 母爱剥夺能引发大鼠抑郁样行为表现,并能抑制纹状体par-4的表达,基因甲基化可能不是其调控机制.
Abstract:
Objective To study the effect of maternal deprivation on the depressive behaviors and the expression of prostate apoptosis response-4(par-4)in adult rats'striatum,and to explore whether DNA methylaion be involved in the regulatory mechanism of par-4 expression.Methods Newborn rats were randomly divided into two groups,the maternal deprivation group rats(n=17)were deprived from their mother 6 hours per day from postnatal day 1 to 14,while the control group rats(n=17)received no experimental handle.When they grew up to thirteen weeks,their depressive level was assessed with forced swimming test and sucrose consumption test,the mRNA expression of par-4 and DRD2 in rats'striatum was detected by real-time Polymerase Chain Reaction(real-time PCR),and the DNA methylation level of par-4 was determined by bisulfated DNA sequencing.Results The float time of maternal deprivation rats [(152.80±74.21)s]was longer than the control rats[(63.80±80.55)s](t=2.79,P<0.05),and the sucrose preference rate of maternal deprivation rats (0.45±0.23)was reduced compared with the control rats(0.69 ±0.25)(t=-2.57,P<0.05).The fold changes of par-4(0.02±0.02)and DRD2(0.11±0.09)mRNA expression in maternal deprivation rats compared to control rats[(0.04±0.02),(0.32±0.21)]were 0.53 and 0.31 respectively.However,there was no significant difference between two groups in methylation level of par-4 promoter region(t=-0.748,P>0.05).Conclusion Maternal deprivation could induce the depressive behavior of rats and influence the expression of par-4,but DNA methylation may not be involved in the regulatory mechanism.  相似文献   

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ABSTRACT - A version of the Geriatric Mental State Examination has been prepared for use in community surveys. Its reliability has been investigated on a sample of geriatric day-patients (n= 52). Two psychiatrists separately examined each patient and audiotaped the interviews. It is argued that unless certain requirements in the data from such a study are fulfilled, interpretable reliability statistics can-not be calculated for individual items. Where the data were sufficient in this study, the mean phi coefficient was 0.84 within interviews and 0.56 between interviews. The reliability of individual items has been assessed as a basis for further improvement in the instrument.  相似文献   

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The use of glutamate antagonists and GABA agonists may protect neurons from the effects of transient ischemia. Felbamate is a new antiepileptic drug with glutamate antagonist and GABA agonist properties, We tested the efficacy of felbamate in a gerbil model of transient forebrain ischemia. Damage assessment was done with silver staining at 7 and 28 days after 5 min of bilateral carotid occlusion, Cerebral cortex, hippocampus (CA1 and CA4), thalamus and striatum were evaluated on a 4-point scoring system, The animals sacrificed at 28 days were also tested in a water-maze task to assess recovery of function, The initial dose of felbamate (300 mg/kg) was given 30 min before the ischemic insult in one set of animals and 30 min after the insult in another set of animals. There were 8 animals tested per group (total: 48 animals). There was significant neuronal protection with the use of felbamate, both before and after ischemia in all regions of the brain. Protection was seen in animals sacrificed at 7 and 28 days, Protection was moderate when felbamate was used before ischemia. It was highly significant when felbamate was given 30 min after the insult. Behavioral studies however did not show any difference in the felbamate treated animals versus the saline treated controls. The structural protection with felbamate was very significant when used in the post-ischemic period. This window for protection merits further evaluation in relation to the clinical setting of stroke.  相似文献   

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Neural circuits in the adult nervous system are characterized by stable, cell type-specific patterns of synaptic connectivity. In many parts of the nervous system these patterns are established during development through initial over-innervation by multiple pre- or postsynaptic targets, followed by a process of refinement that takes place during development and is in many instances activity dependent. Here we report on an identified synapse in the mouse retina, the cone photoreceptor➔type 4 bipolar cell (BC4) synapse, and show that its development is distinctly different from the common motif of over-innervation followed by refinement. Indeed, the majority of cones are contacted by single BC4 throughout development, but are contacted by multiple BC4s through ongoing dendritic elaboration between 1 and 6 months of age—well into maturity. We demonstrate that cell density drives contact patterns downstream of single cones in Bax null mice and may serve to maintain constancy in both the dendritic and axonal projective field.  相似文献   

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背景:睾酮对骨关节炎的作用尚无一致的观点,其调节软骨代谢的作用鲜有文献报道。 目的:观察睾酮对膝骨关节炎雄兔关节软骨中胰岛素样生长因子1表达的影响。 方法:24只雄兔随机分成4组,采用改良Hulth法建立右膝骨关节炎模型;假去势组不切除睾丸,其余3组切除双侧睾丸。第8周末处死假去势组和去势8周组兔取材。第9周开始,激素组肌注生理剂量十一酸睾酮(6 mg/kg, 2周1次),去势16周组正常喂养,并于16周末处死并取材。 结果与结论:大体和组织学观察显示各组兔膝关节软骨的病变程度为假去势组优于去势8周组,激素组优于去势16周组。免疫组化染色显示胰岛素样生长因子1在所有兔膝关节软骨中均有表达,阳性细胞个数假去势组高于去势8周组(P < 0.05),激素组高于去势16周组(P < 0.05),去势8周组与去势16周组差异无显著性意义(P > 0.05)。说明睾酮可通过上调去势雄兔关节软骨中胰岛素样生长因子1的表达,延缓软骨退变。  相似文献   

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Dopaminergic amacrine cells (DACs) release dopamine in response to light‐driven synaptic inputs, and are critical to retinal light adaptation. Retinal degeneration (RD) compromises the light responsiveness of the retina and, subsequently, dopamine metabolism is impaired. As RD progresses, retinal neurons exhibit aberrant activity, driven by AII amacrine cells, a primary target of the retinal dopaminergic network. Surprisingly, DACs are an exception to this physiological change; DACs exhibit rhythmic activity in healthy retina, but do not burst in RD. The underlying mechanism of this divergent behavior is not known. It is also unclear whether RD leads to structural changes in DACs, impairing functional regulation of AII amacrine cells. Here we examine the anatomical details of DACs in three mouse models of human RD to determine how changes to the dopaminergic network may underlie physiological changes in RD. By using rd10, rd1, and rd1/C57 mice we were able to dissect the impacts of genetic background and the degenerative process on DAC structure in RD retina. We found that DACs density, soma size, and primary dendrite length are all significantly reduced. Using a novel adeno‐associated virus‐mediated technique to label AII amacrine cells in mouse retina, we observed diminished dopaminergic contacts to AII amacrine cells in RD mice. This was accompanied by changes to the components responsible for dopamine synthesis and release. Together, these data suggest that structural alterations of the retinal dopaminergic network underlie physiological changes during RD. J. Comp. Neurol. 524:1208–1221, 2016. © 2015 Wiley Periodicals, Inc.  相似文献   

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In the retina, dopamine is a key molecule for daytime vision. Dopamine is released by retinal dopaminergic amacrine cells and transmits signaling either by conventional synaptic or by volume transmission. By means of volume transmission, dopamine modulates all layers of retinal neurons; however, it is not well understood how dopamine modulates visual signaling pathways in bipolar cells. Here we analyzed Drd1a‐tdTomato BAC transgenic mice and found that the dopamine D1 receptor (D1R) is expressed in retinal bipolar cells in a type‐dependent manner. Strong tdTomato fluorescence was detected in the inner nuclear layer and localized to type 1, 3b, and 4 OFF bipolar cells and type 5‐2, XBC, 6, and 7 ON bipolar cells. In contrast, type 2, 3a, 5‐1, 9, and rod bipolar cells did not express Drd1a‐tdTomato. Other interneurons were also found to express tdTomato including horizontal cells and a subset (25%) of AII amacrine cells. Diverse visual processing pathways, such as color or motion‐coded pathways, are thought to be initiated in retinal bipolar cells. Our results indicate that dopamine sculpts bipolar cell performance in a type‐dependent manner to facilitate daytime vision. J. Comp. Neurol. 524:2059–2079, 2016. © 2015 Wiley Periodicals, Inc.  相似文献   

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In Alzheimer's disease, amyloid plaque formation is associated with the focal death of oligodendrocytes and soluble amyloid β impairs the survival of oligodendrocytes in vitro. However, the response of oligodendrocyte progenitor cells (OPCs) to early amyloid pathology remains unclear. To explore this, we performed a histological, electrophysiological, and behavioral characterization of transgenic mice expressing a pathological form of human amyloid precursor protein (APP), containing three single point mutations associated with the development of familial Alzheimer's disease (PDGFB-APPSw.Ind, also known as J20 mice). PDGFB-APPSw.Ind transgenic mice had impaired survival from weaning, were hyperactive by 2 months of age, and developed amyloid plaques by 6 months of age, however, their spatial memory remained intact over this time course. Hippocampal OPC density was normal in P60-P180 PDGFB-APPSw.Ind transgenic mice and, by performing whole-cell patch-clamp electrophysiology, we found that their membrane properties, including their response to kainate (100 µM), were largely normal. However, by P100, the response of hippocampal OPCs to GABA was elevated in PDGFB-APPSw.Ind transgenic mice. We also found that the nodes of Ranvier were shorter, the paranodes longer, and the myelin thicker for hippocampal axons in young adult PDGFB-APPSw.Ind transgenic mice compared with wildtype littermates. Additionally, oligodendrogenesis was normal in young adulthood, but increased in the hippocampus, entorhinal cortex, and fimbria of PDGFB-APPSw.Ind transgenic mice as pathology developed. As the new oligodendrocytes were not associated with a change in total oligodendrocyte number, these cells are likely required for cell replacement.  相似文献   

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