无热惊厥与婴幼儿额叶脑回发育迟缓的CT随访

目的讨论婴幼儿早期无热惊厥与额叶脑回发育落后的CT表现。方法对临床150例无热惊厥患儿出院后随访,选择有完整追踪资料的69例经头颅CT检查诊断为额叶脑回发育迟缓患儿,定期评价至3岁龄。结果额叶发育迟缓及惊厥发作人次均以6-9个月两个年龄组最多,1-3岁3个年龄组随着脑回的发育,惊厥随之减少;所有病例头围与正常同龄儿比较均在正常低限;各种病因导致的脑额叶发育迟缓的恢复时间有区别,低体重儿恢复快,而肠道感染合并中毒性脑病恢复较慢。结论CT可早期直观提示婴儿、幼儿早期额叶脑回发育迟缓情况,为临床早期确诊婴幼儿良性惊厥提供新的诊断信息。     

雌激素替代治疗大鼠海马结构PKC阳性细胞的变化

目的 :观察雌性大鼠行去势后以及雌激素替代治疗海马结构蛋白激酶C ( proteinkinaseC ,PKC)阳性细胞的变化 ,通过该模型研究绝经期后女性情绪烦躁、记忆下降等神经精神症状的分子机制。方法 :将大鼠分为对照组、去势 3个月组和去势后雌激素替代治疗 3个月组 ,用免疫组织化学方法检测海马结构PKC阳性细胞的变化。结果 :PKC阳性细胞主要分布于下托和齿状回的颗粒层 ,其中齿状回内的阳性细胞较下托的多。去势 3个月组与对照组相比 ,齿状回内的PKC阳性细胞没有显著性减少 (P >0 .0 5 ) ,下托PKC阳性细胞显著减少 (P <0 .0 5 ) ;雌激素治疗组与对照组相比 ,下托细胞数量有所减少 ,但无显著性差异 (P >0 .0 5 )。结论 :海马结构下托PKC阳性细胞的减少可能在绝经后女性情绪烦躁、记忆下降等症状中起重要的作用。     

二甲双胍对小鼠衰老过程中学习记忆能力的影响

目的探究D-半乳糖诱导小鼠衰老过程中补充二甲双胍对小鼠学习记忆能力的影响及可能机制。方法将24只雌性ICR小鼠随机分为3组:对照组、衰老组、衰老+二甲双胍组,每组8只,连续给药16周。监测各组小鼠体重及食物摄取量;行为学检测小鼠学习记忆能力;HE染色观察小鼠海马组织结构;比色法检测各组小鼠海马组织中谷胱甘肽(glutathione,GSH)水平。结果与衰老组相比,衰老+二甲双胍组小鼠体重降低(P0.05);Morris水迷宫逃避潜伏期、游泳路程明显减少(P0.01或P0.05),目标象限内游泳时间延长(P0.05),游泳速度加快(P0.05);穿梭实验中主动回避次数升高(P0.05);HE染色显示海马齿状回中核皱缩、深染的海马神经元明显减少;海马组织GSH水平显著升高(P0.05)。结论补充二甲双胍可以明显延缓小鼠衰老过程中学习记忆能力的下降,维持海马神经元正常结构,其机制可能与降低小鼠体重及增强海马组织抗氧化水平有关。     

电针对老年性痴呆模型大鼠海马线粒体酶活性的影响

目的研究电针对老年性痴呆（AD）模型大鼠海码神经元线粒体酶活性的影响，从能量代谢的角度探讨电针治疗AD的部分作用机制。方法以D-半乳糖腹腔注射和Aβ1-40海马注射诱导形成的AD模型大鼠为研究对象，电针“百会”、“涌泉”穴，每日1次，连续20d。以通道式水迷宫测试学习记忆能力的变化，评价电针对AD的治疗效庸；以生化方法检测海马神经元线粒体琥珀酸脱氢酶、Na^＋ -K^＋ -ATP酶、Ca^2＋ -Mg^2＋ -ATP酶的活性。结果电针能有效改善AD模型大鼠学习记忆能力，提高线粒体琥珀酸脱氢酶、Na^＋ -K^＋ -ATP酶、Ca^2＋ -Mg^2＋ -ATP酶活性。结论电针可促进ATP的合成与分解利用，调节线粒体功能，改善AD能量代谢障碍。     

静息态fMRI观察经颅电刺激对睡眠剥夺后青年志愿者后扣带回皮质连接紊乱的干预作用

目的 采用静息态功能MRI（rs-fMRI）观察经颅电刺激（tDCS）对睡眠剥夺（SD）后青年志愿者双侧后扣带回皮质（PCC）功能连接紊乱的干预作用。方法 对16名健康志愿者间隔施加2次24 h SD，随后随机给予真/假tDCS，于正常睡眠清醒休息状态（RW）、SD后及真/假tDCS后采集fMRI数据并进行蒙特利尔认知评估（MoCA），选取双侧PCC作为种子点，计算种子点与全脑间功能连接，观察RW、SD后及真/假tDCS组间功能连接变化，比较MoCA差异。结果 SD后受试者平均MoCA分值较RW减低（t=8.047，P<0.05）；真tDCS后平均MoCA分值（27.06±1.53）高于假tDCS后（25.13±1.86，t=-3.081，P=0.008）和SD后（24.75±2.41，t=3.306，P=0.005）。SD后双侧PCC与双侧丘脑功能连接较RW上升，而与右侧楔前叶功能连接下降。真tDCS后双侧PCC与双侧丘脑间功能连接较假tDCS后下降，而左侧PCC与右侧楔前叶间功能连接上升。结论 24 h SD能引起PCC网络连接紊乱；tDCS对SD所致网络功能连接紊乱具有一定干预作用。     

Neurogenesis impairment and increased cell death reduce total neuron number in the hippocampal region of fetuses with Down syndrome

We previously obtained evidence for reduced cell proliferation in the dentate gyrus (DG) of fetuses with Down syndrome (DS), suggesting that the hippocampal hypoplasia seen in adulthood may be caused by defective early neuron production. The goal of this study was to establish whether DS fetuses (17-21 weeks of gestation) exhibit reduction in total cell number in the DG, hippocampus and parahippocampal gyrus (PHG). Volumes of the cellular layers and cell number were estimated with Cavalieri's principle and the optical fractionator method, respectively. We found that in DS fetuses all investigated structures had a reduced volume and cell number. Analysis of cell phenotype showed that DS fetuses had a higher percentage of cells with astrocytic phenotype but a smaller percentage of cells with neuronal phenotype. Immunohistochemistry for Ki-67, a marker of cycling cells, showed that DS fetuses had less proliferating cells in the germinal zones of the hippocampus and PHG. We additionally found that in the hippocampal region of DS fetuses there was a higher incidence of apoptotic cell death. Results show reduced neuron number in the DS hippocampal region and suggest that this defect is caused by disruption of neurogenesis and apoptosis, two fundamental processes underlying brain building.     

In vivo BDNF modulation of adult functional and morphological synaptic plasticity at hippocampal mossy fibers

The Rho family of small GTPase proteins are involved in the formation and maintenance of neuronal dendrites. In this study, we show that Daam1, a member of the Diaphanous-related formin protein family and a downstream effector for RhoA, is localized to the dendrites of hippocampal neurons. Immunoblot analysis showed that Daam1 is enriched in the mouse hippocampus and co-fractionates in brain lysates with dendritic and synaptic proteins. Immunohistochemical analysis revealed that Daam1 protein distributes in a punctate pattern throughout the cell body and dendritic shafts of dissociated hippocampal neurons and organotypic hippocampal cultures. Although Daam1 is mostly expressed in the shaft of dendrites, co-stainings with SV2 or PSD95 revealed that Daam1 is also present at some synapses. In addition, viral directed expression of a fluorescently tagged Daam1 fusion protein in hippocampal slices resulted in targeted delivery to the dendrites of pyramidal neurons, leading to a reduction in the density of spines.     

Probability discrimination learning in hippocampectomized rats

Rats with hippocampal lesions or neocortical lesions and normal rats were trained on a spatial probability discrimination task where one side of a T maze was reinforced on 70% of the trials and the other side on the remaining 30% of the trials. Training was to a criterion of 39 correct trials out of 40 using a noncorrection procedure. There was no difference between the learning rates of normal rats and with neocortical lesions, but the rats with hippocampal lesions learned the discriminiation more rapidly than the other two groups. These results indicated that the hippocampus does not function as a stimulus gating system, but is probably concerned in the selection and rejection of hypothese (central-sets).     

何首乌饮减轻β-淀粉样蛋白诱导的海马神经元损伤的作用机制

目的 探讨何首乌饮对β 淀粉样蛋白（Aβ）诱导的大鼠原代培养海马神经元损伤保护作用及可能机制。方法 采用新生24h 内的SD大鼠进行原代培养海马神经元,将培养10d的海马神经元分为模型组、何首乌饮保护组、何首乌饮治疗组、何首乌饮对照组及空白对照组。Hoechst33258染色观察海马神经元的凋亡率;免疫组织化学、Western blotting和RT-PCR检测各组海马神经元硫氧还蛋白1（Trx1）蛋白和mRNA的表达情况。 结果 模型组细胞凋亡率增高（P<0.05）,Trx1蛋白和mRNA的表达量明显减少（P<0.05）;与模型组相比,何首乌饮治疗组和预防组的凋亡率明显降低（P<0.05）,Trx1蛋白和mRNA的表达量明显增加（P<0.05）。 结论 何首乌饮可明显减轻Aβ诱导的海马神经元的损伤,其机制可能与增加抗氧化蛋白Trx1的表达有关。     

Hippocampal mossy fiber sprouting is not impaired in brain-derived neurotrophic factor-deficient mice

In human temporal lobe epilepsy, a loss of hilar neurons followed by the sprouting of recurrent mossy fiber collaterals and the reinnervation of free synaptic sites on granule cell dendrites are discussed as possible mechanisms underlying hippocampal hyperexcitability. Dentate granule cells have been shown to upregulate brain-derived neurotrophic factor (BDNF) as well as TrkB, the high-affinity receptor for BDNF, in response to limbic seizures. This raised the possibility that BDNF is an important factor in hippocampal mossy fiber sprouting. Here we have used slice cultures of hippocampus, in which mossy fibers sprout and form a supragranular plexus in response to granule cell deafferentation, and have compared cultures from early postnatal BDNF-deficient mice and wild-type mice. We demonstrate that there is sprouting of supragranular mossy fibers in cultured slices from both BDNF knock-out and wild-type mice. We conclude that BDNF is not an essential factor for mossy fiber sprouting. However, our data do not exclude a role for BDNF in mossy fiber sprouting in wild-type mice, as compensatory mechanisms might have become effective in the mutant. Received: 6 January 1998 / Accepted: 23 February 1998