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1.
在急性、慢性在体大鼠及离体脑片癫癇模型上观察EEG、深部电图、神经元网络及单个神经元的电活动,研究中枢同步化电振荡行为在癫癇发生中的重要作用.实验结果表明:离体脑片(n=40)上强直电刺激海马Schaeffer侧枝,32.5% CA1神经元全细胞记录呈现3～100 Hz膜电位振荡,这种电振荡能促进细胞外场电位癫癇活动形式的转化.急性癫癇模型上(n=10,in vivo),反复强直电刺激海马或中部颞叶新皮质可诱发海马区4～7 Hz和中部颞叶新皮质20 Hz(n=11)深部电图电振荡.慢性强直电刺激大鼠背侧海马(n=12)或中部颞叶新皮质(n=11),7～8 d后出现这些脑区和EEG电振荡活动的频率及幅度的增加.巨大EEG节律性电振荡活动成为电图和癫癇行为性发作的先兆.说明过度激活海马-内嗅皮质-颞叶新皮质产生的同步化电振荡可能是颞叶癫癇发生的重要原因之一. 相似文献
2.
强直电刺激大鼠海马,中部颞叶新皮质诱发癫痫模型中电振？… 总被引：2，自引：0，他引：2
在急性,慢性在体大鼠及体脑片癫痫模型上观察ＥＥＧ、深部电图、神经元网络及单个神经元的电活动,研究中枢同步电振荡行为为在癫痫发生中的重要作用。实验结果表明：离体脑片上强直电刺激海马Ｓｃｈａｅｆｆｅｒ侧枝,３２．５％ＣＡ１神经元全细胞记录呈现３－１００Ｈｚ膜电位振荡,这种电振荡能促进细胞外场电位癫痫活动形式的转化。急性癫痫模型上（ｎ＝１０,ｉｎ ｖｉｖｏ）反复强直电刺激海马或中部颞叶新皮质可诱发海马区 相似文献
3.
强直电刺激大鼠海马-颞叶新皮质神经通路致癫癎放电中突触传递可塑性及其癫癎 靶行为的表达研究(英文) 总被引：3，自引：0，他引：3
强直电刺激诱发大鼠急、慢性在体和离体脑片癫疒间模型。观察癫疒间电活动的突触可塑性以及癫疒间发作的行为表达特征。结果表明 :慢性癫疒间 大鼠原发性湿狗样抖的频率先增加后减少及潜伏期逐步缩短 ,并相继出现继发性湿狗样抖和“点燃”效应 ,称之为行为改变的可塑性 ,即“长时程”效应 ;急性在体癫疒间模型上反复强直电刺激海马 ,颞叶新皮质区细胞外场电位原发性后放的潜伏期逐渐缩短及幅度逐级增大 ,此效应在脑室内微量注射东莨菪碱后逐渐消失 ;离体脑片上强直电刺激海马 Schaeffer侧枝 ,CA1神经元膜电位原发性后放电及阵发性爆发放电的潜伏期明显缩短 ,表现为突触传递的“长时程增强”。推测癫疒间发作行为的可塑性变化可能是复杂神经网络多级突触传递长时程效应的整体靶行为表现。 相似文献
4.
强直电刺激诱发大鼠急、慢性在体和离体脑片癫模型.观察癫电活动的突触可塑性以及癫发作的行为表达特征.结果表明:慢性癫大鼠原发性湿狗样抖的频率先增加后减少及潜伏期逐步缩短,并相继出现继发性湿狗样抖和"点燃”效应,称之为行为改变的可塑性,即"长时程”效应;急性在体癫模型上反复强直电刺激海马,颞叶新皮质区细胞外场电位原发性后放的潜伏期逐渐缩短及幅度逐级增大,此效应在脑室内微量注射东莨菪碱后逐渐消失;离体脑片上强直电刺激海马Schaeffer侧枝,CA1神经元膜电位原发性后放电及阵发性爆发放电的潜伏期明显缩短,表现为突触传递的"长时程增强”.推测癫发作行为的可塑性变化可能是复杂神经网络多级突触传递长时程效应的整体靶行为表现. 相似文献
5.
目的 探讨颞叶癫(癎)大鼠海马组织中miRNA分子表达谱的差异,为进一步研究相关miRNA在颞叶癫(癎)发病机制中的作用打下基础.方法 对同一父系和母系的子代大鼠,利用氯化锂-匹罗卡品化学诱导方法制备慢性颞叶癫(癎)大鼠模型.分别提取1只正常和3只颞叶癫(癎)大鼠海马组织的miRNA,采用高通量的miRNA微阵列芯片杂交,筛选颞叶癫(癎)海马组织中差异表达的内源性miRNA.结果 在大鼠海马组织中共检测到125个miRNA基因.与正常大鼠相比,颞叶癫(癎)大鼠海马组织中差异表达的miRNA有23个,其中有5个miRNA下调,18个miRNA上调.结论 与正常大鼠相比,颞叶癫(癎)大鼠海马组织中存在差异表达的miRNA分子,差异表达的miRNA分子可能参与癫(癎)的发病过程,具有潜在的研究价值. 相似文献
6.
目的 探讨海马有病损的颞叶内侧癫(癎)的手术价值.方法 回顾性分析经手术治疗的15例伴有海马病损颞叶内侧癫(癎)患者.均经详细了解发作症状学、附加蝶骨电极的长程视频脑电图及颅脑磁共振等检查;经正规而详尽的术前评估,行前颞叶切除术,术后随访至少半年以上.结果 术后依据Engel分级,显效(Ⅰ级和Ⅱ级)占80.0％ (12/15)、好转(Ⅲ级)占20.0％(3/15)、无效(Ⅳ级)为0.0％.结论 颞叶内侧癫(癎)手术效果确切,是基层医院开展癫(癎)手术的理想选择. 相似文献
7.
目的:动态观察钠-钙交换体(NCX)mRNA和蛋白在氯化锂-匹罗卡品致(癎)模型大鼠海马CA1、CA3及齿状回区表达的变化,探讨其在癫(癎)发生发展中的作用.方法:用氯化锂-匹罗卡品制备癫(癎)动物模型;应用原位杂交和免疫组化技术检测各时间点NCX3 mRNA和蛋白的表达.结果:急性期(6～24 h)海马各区NCX3 mRNA表达均随时间的延长逐渐减少;进入静止期各区表达趋向回升,慢性反复自发发作期(30、60 d)各区表达又出现不同程度的两次下调.除致(癎)后6 h大鼠海马各区的NCX3蛋白表达无明显变化外,NCX3蛋白变化趋势与NCX3 mRNA基本一致.结论:NCX3表达下调可能通过增加神经元钙超载,改变海马神经元的兴奋性,促使癫(癎)发生. 相似文献
8.
目的 探讨选择性杏仁核海马切除术对治疗颞叶内侧型癫(癎)的疗效.方法 选择颞叶脑电异常与海马硬化同侧病例10例,其中单纯部分性发作继发全身性发作2例,复杂部分性发作5例(3例继发全身性发作),全身强直-阵挛性发作3例.经颞底海马旁回入路切除杏仁核海马.结果 术后病人均恢复良好.所有病例均随访1 a以上,6例发作完全缓解(EngelⅠ、Ⅱ级,60%),2例缓解明显(Engel Ⅲ级,20%),1例轻度缓解(Engel Ⅳ级,10%),1例病人术后半年自行停药造成癫(癎)复发.结论 对伴同侧海马硬化的颞叶内侧型癫(癎)患者行选择性杏仁核海马切除术(经颞底海马旁回入路)疗效显著,可改善性发作情况. 相似文献
9.
目的 总结术中唤醒麻醉下,皮质电刺激(CS)联合皮质脑电图(ECoG)监测治疗功能区肿瘤继发癫(癎)的临床经验.方法 回顾性分析功能区28例胶质瘤及13例脑膜瘤继发癫(癎)病人的临床资料,采用唤醒麻醉下开颅,通过CS定位感觉、运动及语言区,ECoG定位致(癎)区,显微手术切除肿瘤及处理致(癎)灶.结果 术中CS定位功能区33例,阴性8例;ECoG发现致(癎)灶29例,无异常12例.胶质瘤全切21例,次全切7例;脑膜瘤全切12例,次全切1例.术后暂时性神经功能障碍加重或新发障碍25例,均于1个月内恢复.随访41例,时间6个月～5.5年.癫(癎)发作消失29例,明显减少12例.结论 唤醒麻醉下联合CS、ECoG治疗功能区肿瘤继发性癫(癎),能最大限度保护脑功能,安全处理致(癎)灶. 相似文献
10.
目的 比较颞叶癫(癎)患者与健康者认知障碍、海马萎缩的差异,探讨颞叶癫(癎)患者认知障碍与海马萎缩的相关性.方法 随机选取颞叶癫(癎)患者49例和健康对照者20名,神经心理量表评价其认知状态并测量双侧海马体积.结果 与健康者相比,颞叶癫(癎)患者的记忆商(83.2±21.0)和智商(91.0±12.3)显著下降(t=-3.365,-4.291,P=0.001,0.000),双侧海马显著萎缩(P=0.000),不对称指数显著增高(t=3.975,P=0.000),差异有统计学意义.颞叶癫(癎)患者记忆力与癫(癎)病程显著负相关(r=-0.339,P=0-017),左右两侧海马萎缩程度与认知指数均显著负相关(左侧:r=-0.297,P=0.038;右侧:r=-0.305,P=0.033),不对称指数与认知指数显著负相关(r=-0.441,P=0.002).结论 颞叶癫(癎)患者双侧海马的萎缩程度越高、对称性越差,认知损伤也就越显著.海马体积测量可以作为颞叶癫(癎)患者智力下降的评价因子. 相似文献
11.
Braxton A. Norwood Argyle V. Bumanglag Francesco Osculati Andrea Sbarbati Pasquina Marzola Elena Nicolato Paolo F. Fabene Robert S. Sloviter 《The Journal of comparative neurology》2010,518(16):3381-3407
In refractory temporal lobe epilepsy, seizures often arise from a shrunken hippocampus exhibiting a pattern of selective neuron loss called “classic hippocampal sclerosis.” No single experimental injury has reproduced this specific pathology, suggesting that hippocampal atrophy might be a progressive “endstage” pathology resulting from years of spontaneous seizures. We posed the alternative hypothesis that classic hippocampal sclerosis results from a single excitatory event that has never been successfully modeled experimentally because convulsive status epilepticus, the insult most commonly used to produce epileptogenic brain injury, is too severe and necessarily terminated before the hippocampus receives the needed duration of excitation. We tested this hypothesis by producing prolonged hippocampal excitation in awake rats without causing convulsive status epilepticus. Two daily 30‐minute episodes of perforant pathway stimulation in Sprague–Dawley rats increased granule cell paired‐pulse inhibition, decreased epileptiform afterdischarge durations during 8 hours of subsequent stimulation, and prevented convulsive status epilepticus. Similarly, one 8‐hour episode of reduced‐intensity stimulation in Long–Evans rats, which are relatively resistant to developing status epilepticus, produced hippocampal discharges without causing status epilepticus. Both paradigms immediately produced the extensive neuronal injury that defines classic hippocampal sclerosis, without giving any clinical indication during the insult that an injury was being inflicted. Spontaneous hippocampal‐onset seizures began 16–25 days postinjury, before hippocampal atrophy developed, as demonstrated by sequential magnetic resonance imaging. These results indicate that classic hippocampal sclerosis is uniquely produced by a single episode of clinically “cryptic” excitation. Epileptogenic insults may often involve prolonged excitation that goes undetected at the time of injury. J. Comp. Neurol. 518:3381–3407, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
12.
Is mossy fiber sprouting present at the time of the first spontaneous seizures in rat experimental temporal lobe epilepsy? 总被引：2，自引：0，他引：2
The contribution of mossy fiber sprouting to the generation of spontaneous seizures in the epileptic brain is under dispute. The present study addressed this question by examining whether sprouting of mossy fibers is present at the time of appearance of the first spontaneous seizures in rats, and whether all animals with increased sprouting have spontaneous seizures. Epileptogenesis was induced in 16 rats by electrically stimulating the lateral nucleus of the amygdala for 20-30 min until the rats developed self-sustained status epilepticus (SSSE). During and after SSSE, rats were monitored in long-term by continuous video-electroencephalography until they developed a second spontaneous seizure (8-54 days). Thereafter, monitoring was continued for 11 days to follow seizure frequency. The density of mossy fiber sprouting was analyzed from Timm-stained preparations. The density of hilar neurons was assessed from thionin-stained sections. Of 16 rats, 14 developed epilepsy. In epileptic rats, the density of mossy fiber sprouting did not correlate with the severity or duration (115-620 min) of SSSE, delay from SSSE to occurrence of first (8-51 days) or second (8-54 days) spontaneous seizure, or time from SSSE to perfusion (20-63 days). In the temporal end of the hippocampus, the sprouting correlated with the severity of neuronal damage (ipsilateral: r = -0.852, P < 0.01 contralateral: r = -0.748, P < 0.01). The two animals without spontaneous seizures also had sprouting. Increased density of sprouting in animals without seizures, and its association with the severity of neuronal loss was confirmed in another series of 30 stimulated rats that were followed-up with video-EEG monitoring for 60 d. Our data indicate that although mossy fiber sprouting is present in all animals with spontaneous seizures, its presence is not necessarily associated with the occurrence of spontaneous seizures. 相似文献
13.
Friederike Kienzler Braxton A. Norwood Robert S. Sloviter 《The Journal of comparative neurology》2009,515(2):181-196
Prolonged dentate granule cell discharges produce hippocampal injury and chronic epilepsy in rats. In preparing to study this epileptogenic process in genetically altered mice, we determined whether the background strain used to generate most genetically altered mice, the C57BL/6 mouse, is vulnerable to stimulation‐induced seizure‐induced injury. This was necessary because C57BL/6 mice are reportedly resistant to the neurotoxic effects of kainate‐induced seizures, which we hypothesized to be related to strain differences in kainate's effects, rather than genetic differences in intrinsic neuronal vulnerability. Bilateral perforant pathway stimulation‐induced granule cell discharge for 4 hours under urethane anesthesia produced degeneration of glutamate receptor subunit 2 (GluR2)‐positive hilar mossy cells and peptide‐containing interneurons in both FVB/N (kainate‐vulnerable) and C57BL/6 (kainate‐resistant) mice, indicating no strain differences in neuronal vulnerability to seizure activity. Granule cell discharge for 2 hours in C57BL/6 mice destroyed most GluR2‐positive dentate hilar mossy cells, but not peptide‐containing hilar interneurons, indicating that mossy cells are the neurons most vulnerable to this insult. Stimulation for 24 hours caused extensive hippocampal neuron loss and injury to the septum and entorhinal cortex, but no other detectable damage. Mice stimulated for 24 hours developed hippocampal sclerosis, granule cell mossy fiber sprouting, and chronic epilepsy, but not the granule cell layer hypertrophy (granule cell dispersion) produced by intrahippocampal kainate. These results demonstrate that perforant pathway stimulation in mice reliably reproduces the defining features of human mesial temporal lobe epilepsy with hippocampal sclerosis. Experimental studies in transgenic or knockout mice are feasible if electrical stimulation is used to produce controlled epileptogenic insults. J. Comp. Neurol. 515:181–196, 2009. © 2009 Wiley‐Liss, Inc. 相似文献
14.
Functional magnetic resonance imaging (MRI) was used to investigate the hypothesis that memory for a large-scale environment is initially dependent on the hippocampus but is later supported by extra-hippocampal structures (e.g., precuneus, posterior parahippocampal cortex, and lingual gyrus) once the environment is well-learned. Participants were scanned during mental navigation tasks initially when they were newly arrived to the city of Toronto, and later after having lived and navigated within the city for 1 yr. In the first session, activation was observed in the right hippocampus, left precuneus, and postcentral gyrus. The second session revealed activation in the caudate and lateral temporal cortex, but not in the right hippocampus; additional activation was instead observed in the posterior parahippocampal cortex, lingual gyrus, and precuneus. These findings suggest that the right hippocampus is required for the acquisition of new spatial information but is not needed to represent this information when the environment is highly familiar. 相似文献
15.
Behavioral experience changed sodium-dependent high affinity choline uptake (SDHACU) in the hippocampus and frontal cortex. Rats were trained on various behavioral tasks and sacrificed after testing. SDHACU was determined in frontal cortex and hippocampus, areas that receive cholinergic innervation from the nucleus basalis magnocellularis (NBM) and the medial septal area (MSA), respectively. Untrained rats taken directly from their home cages had fairly consistent levels of SDHACU in the hippocampus (1.76 ± 0.45, X ± S.E.) and frontal cortex (1.46 ± 0.37). In the hippocampus of rats performing in a radial maze and T-maze and in rats that surpassed a criterion level in an active avoidance task, SDHACU increased significantly above Cage (untrained) group levels. In the cortex of rats performing the radial maze task, SDHACU decreased slightly. There were no other changes in frontal cortical SDHACU. After behavioral testing ceased, SDHACU in rats performing the radial maze task remained elevated above Control and Treadmill group levels for 20 days, but returned to near control levels 40 days later. Our data demonstrate that a functional differentiation exists between the MSA and NBM cholinergic systems, and that the measurement of SDHACU in central cholinergic neurons is a useful tool to identify the influences of behavior and environment upon changes in neurochemical events and neuronal activity. 相似文献
16.
Benmaamar R Pham-Lê BT Marescaux C Pedrazzini T Depaulis A 《The European journal of neuroscience》2003,18(4):768-774
Neuropeptide Y appears to modulate epileptic seizures differentially according to the receptor subtypes involved. In the hippocampus, neuropeptide Y expression and release are enhanced in different models of epileptogenesis. On the contrary, the expression of Y1 receptors is decreased and it has been shown that activation of these receptors has pro-convulsant effects. The aim of our study was to investigate the role of Y1 receptors during hippocampal kindling epileptogenesis using (i) knock-out mice lacking Y1 receptors and (ii) intrahippocampal infusion of Y1 antisense oligodeoxynucleotide in rats. Y1 knock-out mice showed similar susceptibility to seizure induction and presented no difference in kindling development as compared with their control littermates. Conversely, local hippocampal down-regulation of Y1 receptors during the first week of hippocampal kindling, induced by a local infusion of a Y1 antisense oligodeoxynucleotide, significantly increased seizure threshold intensity and decreased afterdischarge duration. A reverse effect was observed during the week following the infusion period, which was confirmed by a significant decrease in the number of hippocampal stimulations necessary to evoke generalized seizures. At the end of this second week, an up-regulation of Y1 receptors was observed in kindled rats infused with the antisense as compared with the mismatch-treated controls. Our results in the rat suggest that the down-regulation of Y1 receptors in the hippocampus participates in the control of the initiation of epileptogenesis. The lack of an effect of the deficiency of Y1 receptors in the control of kindling development in Y1 knock-out mice could be due to compensatory mechanisms. 相似文献
17.
The hippocampus is a brain region that is critical for spatial learning, context‐dependent memory, and episodic memory. It receives major inputs from the medial entorhinal cortex (MEC) and the lateral EC (LEC). MEC neurons show much greater spatial firing than LEC neurons in a recording chamber with a single, salient landmark. The MEC cells are thought to derive their spatial tuning through path integration, which permits spatially selective firing in such a cue‐deprived environment. In accordance with theories that postulate two spatial mapping systems that provide input to the hippocampus—an internal, path‐integration system and an external, landmark‐based system—it was possible that LEC neurons can also convey a spatial signal, but that the signal requires multiple landmarks to define locations, rather than movement integration. To test this hypothesis, neurons from the MEC and LEC were recorded as rats foraged for food in cue‐rich environments. In both environments, LEC neurons showed little spatial specificity, whereas many MEC neurons showed a robust spatial signal. These data strongly support the notion that the MEC and LEC convey fundamentally different types of information to the hippocampus, in terms of their spatial firing characteristics, under various environmental and behavioral conditions. © 2010 Wiley Periodicals, Inc. 相似文献
18.
The hippocampus is widely considered to be a critical component of a medial temporal lobe memory system, necessary for normal performance on tests of declarative memory. Object recognition memory is thought to be a classic test of declarative memory function. However, previous tests of the effects of hippocampal lesions on object recognition memory have not always supported this view. One possible reason for this inconsistency is that previously reported effects of hippocampal lesions on object recognition memory tasks may have stemmed not from a deficit in object recognition memory per se, but as a result of spatial and contextual confounds in the task. Thus, in the present study, we used a spontaneous object recognition test in a modified apparatus designed to minimize spatial and contextual factors. A group of rats with complete excitotoxic lesions of the hippocampus and a group of control rats were tested on this modified spontaneous object recognition task with retention delays of up to 48 h. These rats were also tested on a spatial nonmatching-to-place task. Spatial memory performance was abolished following hippocampal lesions, whereas performance on the recognition memory task was intact at all delays tested. 相似文献
