海马后的

The rats were killed in 0,24,48 and 72 hours after hypoxic-ischemia to detect the level of SOD and NDA in rat brain and neuronal apoptosis in the hippocampal CAI regin was detected by HE and TUNEL staining.

于手术后即刻，②、③于处置后0、24、48、72h断头取脑，分别检测SOD/MDA的水平，并经HE和Tunel染色，光镜下检测海马CAI脑细胞凋亡数。

Using the intracellular recording technique for monitoring the excitatory postsynaptic potentials of CA1 pyramidal neuron and delivering an activator of protein kinase C and/or inhibitors of PKC and 〓/calmodulin-dependent protein kinase Ⅱ into postsynaptic cell in hippocampal slices, we studied the role of postsynaptic PKC and CaMKⅡ in long-term potentiation induced by high frequency stimulation at the CA1 synapses made by Schaffer collateral/commissural and perforant pathway afferents.

用电生理学方法在大鼠海马脑片CA1区锥体细胞记录Schaffer侧枝和穿通通路到CA1神经元突触的兴奋性突触后电位，通过送蛋白激酶抑制剂和激活剂进入突触后细胞，我们研究了突触后蛋白激酶C和依赖钙/钙调蛋白的Ⅱ型蛋白激酶在高频刺激诱导的长时程增强产生和维持中的作用。

Meanwhile, in the CA3 area of hippocampus in NS group, a small amount of N-Cadherin positive cells were visible and were slightly stained. Compared with NS group, in PTZ seizure group, N-Cadherin positive cells had a marked increase in area CA3 and dentate hilus (P.01), but they were strongly inhibited in PDTC group (P.05). There was no correlation between the expressions of N-cadherin, Timm-stained granules and between the age of rats with seizure.

同时，NS组14天和28天大鼠海马CA3区可见少量的N-Cadherin阳性细胞，着色不深；PTZ致惊组海马CA3和齿状回门区的N-Cadherin阳性细胞与NS组相比明显增多（P＜0.01），PDTC预处理后相同区域内N-Cadherin阳性细胞较PTZ致惊组明显减少（P＜0.05）。N-Cadherin与Timm染色颗粒的表达结果与惊厥鼠的日龄并无关联性。

Consequently, studying the effect of aluminium on Long-TermPotentiation and approaching its possible mechanisms can elucidate the mechanisms ofaluminium on study and memory. The research indicated that the pregnant and lactational stage is the importantstage for the filial brain growth and development.

因此本次实验采用整体动物实验的方法，通过对大鼠孕哺期慢性铝暴露，以子代大鼠海马为研究对象，探讨大鼠孕哺期铝暴露后对其子代大鼠海马LTP形成、维持的影响，并从蛋白激酶C表达的途径为阐明铝影响LTP的机制提供思路。

The therapy groups displayed significant improvements in neuromotor functions and survivals of neuron and oligodendrocyte compared with control groups. These results demonstrated the neuroprotect roles of GGF2, and cationic liposome-mediated GGF2 transgene therapy has potential possibility.

结果：1、大鼠LFP致伤后3—7天，GGF2 mRNA在海马CAl区、CA2区、CA3区、DG及皮层表达明显增加。2、阳离子脂质体介导GGF2转基因治疗可促进大鼠伤后行为学的恢复，可促进损伤区神经元及少突胶质细胞的存活。3、原核表达方法得到GGF2重组蛋白。

Mutant mice than in wild-type controls, and tetrodotoxin or bicuculline application abolished the difference between the genotypes. Studies on human oligodendroglioma cells revealed that GABA played a protective role on Ca〓 overload induced by OGD or glutamate and phaclofen, GABA〓 receptor antagonist, could significantly block the protection.

结果表明：①电凝大脑中动脉后Ca〓2.3-／-鼠脑梗死率和缺血后运动障碍明显重于Ca〓2.3+／+鼠；②Ca〓2.3-／-鼠海马脑片CA1区缺氧后钙超载明显高于Ca〓2.3+／+鼠；③Na〓通道阻滞剂TTX和GABA〓受体阻断剂bicuculline可显著缩小遗传表型之间的差异；④GABA对缺氧无糖及谷氨酸所致的人胶质细胞瘤细胞Ca〓超载有明显的保护作用，此作用可被GABA〓受体阻断剂phaclofen拮抗。

To elucidate the molecular mechanisms underlying the neural plasticity after CNS injury, the gene expression profile in the rat hippocampus following perforant path transections was explored by several methods including custom differential screening, custom cDNA array and cDNA microarray.

为了阐明中枢神经系统损伤后神经可塑性的分子机制，本实验探索了多种方法，包括传统差异筛库、传统cDNA array和cDNA microarray，对穿通纤维切断后大鼠海马的基因表达图谱进行了研究。

There were no statistically differences between the 8th~ 14thday, the 15th - 21th day post-BC and the control group. During the rt~24tkday post-BC , pycnosis degeneration or necrosis neurons of the locus cerebral cortex, dorsal hippocampus, dentate fornix were significantly increased, then decreased gradually, but recovered to normal by the 24thday after BC, and especially in parietal cortex and piriform cortex the necrosis neurons were significantly increased than temporal cortex , and there were no statistically difference berween the left and the right side. Pycnosis degeneration or necrosis neurons in the brainstem reticular formation were markedly increased in the 4thday after BC, and there were no statistically difference among the other groups and the control group.

与对照组相比，BC后在大脑皮质、背侧海马和齿状回部位，固缩变性和不完全坏死细胞数先显著增加(P＜0.05)，然后逐渐减少，至24d基本恢复正常；顶叶、梨状皮质比颞叶皮质变性坏死细胞多，差异有高度显著性(P＜0.01)；大脑左侧比右侧变性坏死细胞稍少但差异无显著性；在BC后4d，脑桥核、斜方体核平面的脑干网状结构中固缩变性和不完全坏死细胞数明显增多(P＜0.05)，其它组间无显著性差异。

Objective To investigate the changes and significances of neurocytes apoptosis and serum nerve growth factor after cerebral contusions.

目的 探讨大鼠脑挫裂伤后海马区神经细胞凋亡及血清神经生长因子的变化及意义方法按照改良Feeney自由落体脑损伤模型方式制作大鼠左顶叶脑挫裂伤模型，应用酶联免疫吸附法和原位细胞凋亡法，分别对脑挫裂伤后0.5，1，3，6，12，24，72，120，168，240h各时相点血清NGF含量及脑组织细胞凋亡进行检测。

The extracellular amino acid neurotransmission levels in hippocampus of free-moving rats were detected by microdialysis with HPLC.3. Results:(1) The extracellular GAB A concentration in the CA1 area decreased immediately after the administration of PTZ but increased at about 3d after PTZ injection and lasted about 2 weeks. However, Glu level increased remarkably after the PTZ injection and decreased at 3d until 14d after PTZ injection.

结果： (1)在发作期，细胞外液GABA的浓度为38119.7±912.7nmol／L，较发作前明显下降，在发作后3天升高，发作后14天仍有升高；而Glu的浓度在发作期为4742.0±201.2nmol／L，较发作前升高，在发作后3天下降，瘫痛大鼠海马区细胞外液氨基酸的动态变化和托毗酷对癫痛大鼠辛l〕经元损伤的保护作用中文提要在发作后14天仍低于发作期。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。