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排序方式: 共有1511条查询结果,搜索用时 78 毫秒
1.
The Pilocarpine Model of Epilepsy in Mice   总被引:29,自引:3,他引:26  
Summary: Purpose : To characterize the acute and chronic behavioral, electrographic and histologic effects of sustained seizures induced by pilocarpine in mice.
Methods : After status epilepticus, the surviving animals were continuously monitored for 24 h/day for 120 days. The brains were processed by using neo-Timm and Nissl stains.
Results : The first spontaneous seizures occurred between 4 and 42 days after status epilepticus. The mean "seizure-silent period" lasted for 14.4 ± 11.9 days. During the chronic phase, recurrent spontaneous seizures were observed 1–5 times per animal per week and were associated with sprouting in the supragranular layer of the dentate gyrus.
Conclusions : Structural brain damage promoted by pilocar-pine-induced status epilepticus may underlie or be associated with recurrent spontaneous seizures in mice.  相似文献
2.
Axonopathy and amyotrophy in mice transgenic for human four-repeat tau protein   总被引:21,自引:4,他引:17  
Coding region and intronic mutations in the tau gene cause frontotemporal dementia and parkinsonism linked to chromosome 17. Some of these mutations lead to an overproduction of tau isoforms with four microtubule-binding repeats. Here we have expressed the longest four-repeat human brain tau isoform in transgenic mice under the control of the murine Thy1 promoter. Transgenic mice aged 3 weeks to 25 months overexpressed human tau protein in nerve cells of brain and spinal cord. Numerous abnormal, tau-immunoreactive nerve cell bodies and dendrites were seen. In addition, large numbers of pathologically enlarged axons containing neurofilament- and tau-immunoreactive spheroids were present, especially in spinal cord. Signs of Wallerian degeneration and neurogenic muscle atrophy were observed. When motor function was tested, transgenic mice showed signs of muscle weakness. Taken together, these findings demonstrate that overexpression of human four-repeat tau leads to a central and peripheral axonopathy that results in nerve cell dysfunction and amyotrophy. Received: 28 September 1999 / Revised, accepted: 18 November 1999  相似文献
3.
Molecular basis of aggression   总被引:19,自引:0,他引:19  
Recent pharmacological and genetic studies have dramatically expanded the list of neurotransmitters, hormones, cytokines, enzymes, growth factors, and signaling molecules that influence aggression. In spite of this expansion, serotonin (5-HT) remains the primary molecular determinant of inter-male aggression, whereas other molecules appear to act indirectly through 5-HT signaling. We review evidence of interactions among these molecules and aggressive behavior. Slight modulations in 5-HT levels, turnover, and metabolism, or in receptor subtype activation, density, and binding affinity affect aggression. Activation of specific 5-HT receptors evokes distinct, but highly interacting, second messenger systems and multiple effectors. Understanding the interactions between 5-HT receptor subtypes should lead to novel insights into the molecular mechanisms of aggression.  相似文献
4.
A Review of Mouse Mutants as Genetic Models of Epilepsy   总被引:18,自引:8,他引:10  
5.
骨髓干细胞移植治疗Duchenne型肌营养不良鼠的实验研究   总被引:17,自引:2,他引:15  
目的 研究骨髓干细胞移植治疗Duchenne型肌营养不良鼠 (mdx鼠 )的效果。方法 取 4~ 5周龄昆明鼠骨髓干细胞 ,体外培养 3d ,静脉移植到 7Gyγ射线预处理 7~ 8周龄mdx鼠体内。临床监测受体鼠移植物抗宿主病 (GVHD)表现 ,并对移植 12周mdx鼠的运动功能、肌电生理、dystrophin蛋白表达情况进行检测。 结果  5只 7Gy剂量放疗mdx鼠 ,静脉移植 4 8× 10 6骨髓干细胞 ,3个月后 ,肌电图指标有了部分改善 ;10 %肌纤维表达了dystrophin蛋白。结论 静脉移植同种非同系鼠骨髓干细胞治疗mdx鼠有效 ,显示骨髓干细胞移植治疗DMD有着理想的前景。  相似文献
6.
Advances in the management of pediatric brain tumors have increased survival rates in children, but their quality of life is impaired due to cognitive deficits that arise from irradiation. The pathogenesis of these deficits remains unknown, but may involve reduced neurogenesis within the hippocampus. To determine the acute radiosensitivity of the dentate subgranular zone (SGZ), 21-day-old C57BL/J6 male mice received whole brain irradiation (2-10 Gy), and 48 h later, tissue was assessed using immunohistochemistry. Proliferating SGZ cells and their progeny, immature neurons, were decreased in a dose-dependent fashion. To determine if acute changes translated into long-term alterations in neurogenesis, mice were given a single dose of 5 Gy, and 1 or 3 months later, proliferating cells were labeled with 5-bromo-2'-deoxyuridine (BrdU). Confocal microscopy was used to determine the percentage of BrdU-labeled cells that showed mature cell phenotypes. X-rays significantly reduced the production of new neurons at both time points, while glial components showed no change or small increases. Measures of activated microglia and infiltrating, peripheral monocytes indicated that reduced neurogenesis was associated with a chronic inflammatory response. Three months after irradiation, changes in neurogenesis were associated with spatial memory retention deficits determined using the Morris water maze. Behavioral training and testing increased the numbers of immature neurons, most prominently in irradiated animals. These data provide evidence that irradiation of young animals induces a long-term impairment of SGZ neurogenesis that is associated with hippocampal-dependent memory deficits.  相似文献
7.
Nitrotyrosine produced by NO-mediated reaction is a possible marker for cytotoxicity in brain ischemia. In this study, we aimed to determine whether iNOS is responsible for the nitrotyrosine formation and which type of cell is predominantly nitrated. Fifty-eight wild-type and 28 iNOS knockout male mice were used. Under halothane anesthesia the left middle cerebral artery was occluded for 2 h and reperfused for 0.5 or 15 h. The ratio of nitrotyrosine to total tyrosine (%NO2-Tyr) was measured by means of a hydrolysis/HPLC. After 0.5-h reperfusion, %NO2-Tyr in the ischemic cortex of wild-type and knockout mice amounted to 0.037 +/- 0.040% (n = 8) and 0.064 +/- 0.035% (n = 6), respectively, being significantly higher than that in the sham operation group (n = 7) (P < 0.05). After 15-h reperfusion, nitrotyrosine was detected only in wild-type mice (0.039 +/- 0.025%, n = 7), not in knockout or sham-operated mice (P < 0.05). Immunohistochemical reaction for nitrotyrosine was seen predominantly in the vascular wall in the peri-infarct region of the cerebral cortex in wild-type mice after 15-h reperfusion, but not in corresponding knockout mice. Our data suggest that iNOS is responsible for nitrotyrosine formation in the later phase of reperfusion, and that vascular endothelium is the major site of this reaction, at least in the case of 15-h reperfusion.  相似文献
8.
Duchenne肌营养不良模型鼠骨髓移植后dystrophin的表达   总被引:17,自引:1,他引:16  
目的 观察Duchenne型肌营养不良模型鼠 (mdx鼠 )不同成分骨髓细胞移植后dystrophin的表达。方法 用体外培养的C57BL雄鼠的骨髓细胞、骨髓悬浮细胞、骨髓基质细胞分别经鼠尾静脉注射到放疗后的mdx鼠体内 ,动态观察受体雌性mdx鼠骨骼肌dystrophin的表达 ,并取受体mdx雌鼠血 ,用聚合酶链反应进行Sry基因检测。结果 骨髓细胞、悬浮细胞、基质细胞移植后 1~ 2个月 ,较少肌纤维表达dystrophin(<1 % ) ,3~ 4个月分别约有 7%、6 %、4 %的肌纤维表达dystrophin。Sry基因检测均扩增出受体雌鼠Y染色体上 449bp的DNA片段 ,提示供体细胞在受体内存活。结论 骨髓细胞、悬浮细胞、基质细胞分别移植到mdx鼠体内后 ,mdx鼠骨骼肌均有dystrophin的表达  相似文献
9.
小鼠记忆保持能力与海马CA3区突触界面结构的相关性   总被引:16,自引:0,他引:16  
本实验对记忆保持(retention)良好组和低劣组小鼠海马CA3区GrayI型突触界面结构进行了定量观察分析,结果表明,记忆保持良好海马CA3区突触后膜致密物质(post-synapticdensity,PSD)极显著地密于记忆保持低劣组(P〈0.01),同时,记忆良好的出现了穿孔性突触(perforatedsynapse)而记忆低劣组没有出现,此外,还测量了突触界面曲率,突触活性区长度和突触间  相似文献
10.
目的 用髓鞘蛋白脂质蛋白多肽(PLP)139-151诱发实验性自身免疫性脑脊髓炎(EAE)小鼠模型。方法 应用PLP139-151抗原加完全福(氏)佐剂免疫SWXJ小鼠。结果 免疫14-20d后小鼠即发病,发病率为80%,而且多数呈缓解-复发型。病理学证实发病小鼠脑和脊髓内具有典型的脱髓鞘改变和炎性细胞浸润。结论 以PLP139-151为抗原免疫SWXJ小鼠诱发EAE,具有模型稳定、发病率高和缓解-复发的特点,是研究多发性硬化较理想的动物模型。  相似文献
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