Resilience to structural and molecular changes in excitatory synapses in the hippocampus contributes to cognitive function recovery in Tg2576 mice

Plaques of amyloid-β(Aβ)and neurofibrillary tangles are the main pathological characteristics of Alzheimer’s disease(AD).However,some older adult people with AD pathological hallmarks can retain cognitive function.Unraveling the factors that lead to this cognitive resilience to AD offers promising prospects for identifying new therapeutic targets.Our hypothesis focuses on the contribution of resilience to changes in excitatory synapses at the structural and molecular levels,which may underlie healthy cognitive performance in aged AD animals.Utilizing the Morris Water Maze test,we selected resilient(asymptomatic)and cognitively impaired aged Tg2576 mice.While the enzyme-linked immunosorbent assay showed similar levels of Aβ42 in both experimental groups,western blot analysis revealed differences in tau pathology in the pre-synaptic supernatant fraction.To further investigate the density of synapses in the hippocampus of 16-18 month-old Tg2576 mice,we employed stereological and electron microscopic methods.Our findings indicated a decrease in the density of excitatory synapses in the stratum radiatum of the hippocampal CA1 in cognitively impaired Tg2576 mice compared with age-matched resilient Tg2576 and non-transgenic controls.Intriguingly,through quantitative immunoelectron microscopy in the hippocampus of impaired and resilient Tg2576 transgenic AD mice,we uncovered differences in the subcellular localization of glutamate receptors.Specifically,the density of GluA1,GluA2/3,and mGlu5 in spines and dendritic shafts of CA1 pyramidal cells in impaired Tg2576 mice was significantly reduced compared with age-matched resilient Tg2576 and non-transgenic controls.Notably,the density of GluA2/3 in resilient Tg2576 mice was significantly increased in spines but not in dendritic shafts compared with impaired Tg2576 and non-transgenic mice.These subcellular findings strongly support the hypothesis that dendritic spine plasticity and synaptic machinery in the hippocampus play crucial roles in the mechanisms of cognitive resilience in Tg2576 mice.

Polyculture of the lined seahorse,Hippocampus erectus Perry,1810 with two species of macroalgae in aquaria

A two-month study was conducted to test the effects of macroalgae on the growth and survivorship of juvenile lined seahorse （Hippocarapus erectus） in aquaria. Twenty-day old seahorses were cultured in the tanks with green alga Chaetomorpha linum, red alga Gracilaria tikvahiae, green plastic artificial plant （stargrass）, and black plastic net, respectively. Increases in wet mass and standard length for the seahorses were significantly higher in the tanks with macroalgae than those without macroalgae. The seahorse survivorships in the two macroalgal treatments were also significantly higher than those of the two treatments without macroalgae. In the treatments with macroalgae, the DO and pH were higher than those without marcoalgae. During the experiment, the color of seahorses was changed to certain extent. In the green background （the treatments with C. linum and stargrass）, 24.1% 28.4% of black seahorses decreased over time; whereas in the black （plastic net） or brown （G. tikvahiae） background treatments, 14.1% 16.3% of yellow seahorses decreased over time, for matching that of the background. Furthermore, the survival rate of seahorse was correlation with DO and pH, and strong correlation with standard length, wet mass and CF. Polyculture with macroalgae, survival rates of seahorse were higher than without macroaglae.

Roles of interleukins in antibacterial immune defense of the brood pouch in the lined seahorse Hippocampus erectus

Seahorse embryos are brooded in the enclosed nutrient-rich environment of the male brood pouch,which may be prone to bacterial infection.The immune responses of interleukin(IL)genes in the brood pouch have not been well studied.We identifi ed 13 interleukins in the lined seahorse Hippocampus erectus.Tissue-specifi c expression analysis revealed increased mRNA expression levels of il-1β,il-18,and il-8 in the brood pouch.When challenged with lipopolysaccharide or Vibrio parahaemolyticus,il-1βand il-18 were active as part of the acute and chronic infl ammatory responses,respectively.Importantly,il-8 may be involved in powerful antibacterial immune responses and may be induced by il-1βand il-18 via a process involving the nuclear factor-κB signaling pathway.These results suggest that il-1β,il-18,and il-8 may play key roles in the antibacterial immune defense of the brood pouch in male seahorses.

Genome-wide evolution of MAPKs family and their expression in response to bacterial infection in seahorse Hippocampus erectus

Seahorses have evolved many unique biological traits,including a male brood pouch,the absence of caudal and pelvic fins,and the lack of spleen and gut-associated lymphatic tissue.The mitogenactivated protein kinases(MAPKs)are known to be involved in various important biological processes including growth,differentiation,immunity,and stress responses.Therefore,we hypothesized that the adaptive evolution and expression of the MAPK gene family in seahorse may differ from those of other teleost species.We identified positive selection sites in the erk2,erk5,jnk1,and p38αMAPK genes of the lined seahorse Hippocampus erectus and tiger-tailed seahorse Hippocampus comes.A novel expression profile of MAPK cascade genes was found in seahorse larvae during the first day after birth based on the RNA-seq data of H.erectus,which refl ected vital signs of immune response to its parental immune system.The expression patterns of the four positively selected MAPK genes were analyzed following the bacterial challenge of Vibrio fortis,revealing their upregulation pattern in brood pouch and other immune tissues.This study enriched our knowledge of the evolution of the H.erectus MAPK subfamilies,and could help better understanding the functional role of MAPKs in teleosts.

Do tau-synaptic long-term depression interactions in the hippocampus play a pivotal role in the progression of Alzheimer’s disease?

Cognitive decline in Alzheimer’s disease correlates with the extent of tau pathology,in particular tau hyperphosphorylation that initially appears in the transentorhinal and related regions of the brain including the hippocampus.Recent evidence indicates that tau hyperphosphorylation caused by either amyloid-βor long-term depression,a form of synaptic weakening involved in learning and memory,share similar mechanisms.Studies from our group and others demonstrate that long-term depression-inducing low-frequency stimulation triggers tau phosphorylation at different residues in the hippocampus under different experimental conditions including aging.Conversely,certain forms of long-term depression at hippocampal glutamatergic synapses require endogenous tau,in particular,phosphorylation at residue Ser396.Elucidating the exact mechanisms of interaction between tau and long-term depression may help our understanding of the physiological and pathological functions of tau/tau(hyper)phosphorylation.We first summarize experimental evidence regarding tau-long-term depression interactions,followed by a discussion of possible mechanisms by which this interplay may influence the pathogenesis of Alzheimer’s disease.Finally,we conclude with some thoughts and perspectives on future research about these interactions.

Quantitative proteomic and phosphoproteomic analyses of the hippocampus reveal the involvement of NMDAR1 signaling in repetitive mild traumatic brain injury

The cumulative damage caused by repetitive mild traumatic brain injury can cause long-term neurodegeneration leading to cognitive impairment.This cognitive impairment is thought to result specifically from damage to the hippocampus.In this study,we detected cognitive impairment in mice 6 weeks after repetitive mild traumatic brain injury using the novel object recognition test and the Morris water maze test.Immunofluorescence staining showed that p-tau expression was increased in the hippocampus after repetitive mild traumatic brain injury.Golgi staining showed a significant decrease in the total density of neuronal dendritic spines in the hippocampus,as well as in the density of mature dendritic spines.To investigate the specific molecular mechanisms underlying cognitive impairment due to hippocampal damage,we performed proteomic and phosphoproteomic analyses of the hippocampus with and without repetitive mild traumatic brain injury.The differentially expressed proteins were mainly enriched in inflammation,immunity,and coagulation,suggesting that non-neuronal cells are involved in the pathological changes that occur in the hippocampus in the chronic stage after repetitive mild traumatic brain injury.In contrast,differentially expressed phosphorylated proteins were mainly enriched in pathways related to neuronal function and structure,which is more consistent with neurodegeneration.We identified N-methyl-D-aspartate receptor 1 as a hub molecule involved in the response to repetitive mild traumatic brain injury,and western blotting showed that,while N-methyl-D-aspartate receptor 1 expression was not altered in the hippocampus after repetitive mild traumatic brain injury,its phosphorylation level was significantly increased,which is consistent with the omics results.Administration of GRP78608,an N-methyl-D-aspartate receptor 1 antagonist,to the hippocampus markedly improved repetitive mild traumatic brain injury-induced cognitive impairment.In conclusion,our findings suggest that N-methyl-D-aspartate receptor 1 signaling in the hippocampus is involved in cognitive impairment in the chronic stage after repetitive mild traumatic brain injury and may be a potential target for intervention and treatment.

SC-Net:A New U-Net Network for Hippocampus Segmentation

Neurological disorders like Alzheimer’s disease have a significant impact on the lives and health of the elderly as the aging population con-tinues to grow.Doctors can achieve effective prevention and treatment of Alzheimer’s disease according to the morphological volume of hippocam-pus.General segmentation techniques frequently fail to produce satisfactory results due to hippocampus’s small size,complex structure,and fuzzy edges.We develop a new SC-Net model using complete brain MRI images to achieve high-precision segmentation of hippocampal structures.The proposed network improves the accuracy of hippocampal structural segmentation by retaining the original location information of the hippocampus.Extensive experimental results demonstrate that the proposed SC-Net model is signif-icantly better than other models,and reaches a Dice similarity coefficient of 0.885 on Alzheimer’s Disease Neuroimaging Initiative(ADNI)dataset.

温度突变对大海马(Hippocampus kuda)幼体生长、组分及酶活力的影响

以大海马幼体为实验材料,通过设置不同的温度突变组(温度从23℃突变至15℃、28℃和33℃)的方法,对其生长、生化组分以及酶活力的影响进行了研究。结果表明,实验结束后,28℃温度组的大海马幼体生长指标、蛋白含量、能值显著高于23℃对照组(P<0.05),而15℃、33℃温度组的各项指标则显著低于对照组(P<0.05);此外,温度突变组的大海马幼体的酶活力均有先升后降的趋势,在1d后出现峰值,4—6d各个温度组趋于稳定,到实验第15天时,28℃温度组的SOD、ACP活力和MDA的含量已处于23℃对照组水平(P>0.05),CAT、AKP活力显著高于23℃对照组(P<0.05)。而15℃、33℃温度组的SOD、CAT活力降至低于23℃对照组水平(P<0.05),15℃温度组的ACP、AKP活力则低于23℃对照组水平(P<0.05),MDA的含量在15℃、33℃温度组随时间延长而增加。

盐度胁迫对大海马(Hippocampus kuda)幼体生长、组分及酶活力的影响

在盐度为25的条件下,以大海马幼体为实验材料,通过设置不同的盐度胁迫组(盐度从25胁迫至5、15和35)的方法,对其生长、生化组分以及酶活力的影响进行了研究。结果表明:15盐度组大海马幼体的体重、生化组分、能值与对照组(盐度25)相比差异不显著(P>0.05),体长、成活率指标则显著高于对照组(P<0.05),然而5、35盐度组的生长指标、成活率、生化组分等则显著低于对照组(P<0.05)。15盐度组的SOD、CAT酶活性低于对照组水平(P<0.05),MDA的含量变化不显著(P>0.05);而5、35盐度组SOD、CAT和MDA含量与对照组相比,随着时间的延长,呈现逐渐升高的趋势(P<0.05);随着盐度的升高,AKP酶活性具有逐渐升高的趋势,而ACP酶活性则呈现降低趋势。

利用Seahorse XF-96探讨不同细胞浓度和血清对线粒体功能的影响

目的利用Seahorse XF-96探讨不同细胞浓度和血清对HUVEC细胞和U87细胞线粒体功能的影响。方法利用细胞线粒体应激试剂盒,在不同浓度的HUVEC细胞和U87细胞中加入抑制剂(寡霉素、解偶联剂、鱼藤酮和抗霉素A),根据细胞浓度分为2000组、4000组、6000组和8000组,根据有无血清和不同的解偶联剂浓度分为血清+低解偶联剂组、血清+高解偶联剂组、无血清+低解偶联剂组和无血清+高解偶联剂组。在Seahorse XF-96中测定线粒体的耗氧率(OCR)和细胞外酸化率(ECAR),并比较HUVEC细胞和U87细胞各组线粒体的基础氧耗、质子漏、最大呼吸能力、非线粒体的氧耗、储备的呼吸能力、三磷酸腺苷(ATP)生成能力、线粒体呼吸潜力和偶联效率;比较HUVEC细胞和U87细胞之间上述指标的差异;观察血清和解偶联剂浓度对HUVEC细胞线粒体功能的影响。结果在HUVEC细胞和U87细胞中,2000组OCR显著低于4000组、6000组和8000组(P<0.01);2000组的ECAR显著低于4000组(P<0.01),4000组显著低于6000组和8000组(P<0.01)。在HUVEC细胞中,与2000组比较,6000组和8000组的基础氧耗、储备的呼吸能力、ATP生成能力和最大呼吸能力增强(P<0.05),8000组非线粒体的氧耗和质子漏增强(P<0.05);在U87细胞中,与2000组比较,6000组和8000组的基础氧耗、非线粒体的氧耗和最大呼吸能力增强(P<0.05),8000组ATP生成能力、储备的呼吸能力和质子漏增强(P<0.05);HUVEC细胞和U87细胞各组间线粒体的偶联效率和线粒体呼吸潜力比较差异均无统计学意义(P>0.05)。U87细胞8000组的质子漏高于HUVEC细胞(P<0.05);HUVEC细胞2000组、6000组和8000组的偶联效率高于U87细胞(P<0.05);HUVEC细胞6000组的ATP生成能力和储备的呼吸能力高于U87细胞(P<0.05);HUVEC细胞和U87细胞各组基础氧耗、最大呼吸能力、非线粒体的氧耗、线粒体呼吸潜力比较差异均无统计学意义(P>0.05)。血清+低解偶联剂组储备的呼吸能力和线粒体呼吸潜力高于无血清+低解偶联剂组(P<0.05),其余指标组间比较差异均无统计学意义(P>0.05);血清+高解偶联剂组和无血清+高解偶联剂组的线粒体功能各指标差异均无统计学意义(P>0.05)。结论随着细胞浓度的不断增加,HUVEC细胞和U87细胞的OCR和ECAR不断升高,细胞浓度会影响两种细胞线粒体的OCR和ECAR,HUVEC细胞和U87细胞的质子漏和偶联效率存在显著差异,血清会影响HUVEC细胞线粒体储备的呼吸能力和线粒体呼吸潜力。

Microinjection of M_5 muscarinic receptor antisense oligonucleotide into VTA inhibits FosB expression in the NAc and the hippocampus of heroin sensitized rats

Objective To investigate the effect of M5 muscarinic receptor subtype on the locomotor sensitization induced by heroin priming, and it＇s effect on the FosB expression in the nucleus accumbens （NAc） and the hippocampus in the heroin sensitized rats. Methods Locomotor activity was measured every 10 min for 1 h after subcutaneous injection of heroin. FosB expression was assayed by immunohistochemistry, and the antisense oligonucleotides （AS-ONs） targeting M5 muscarinic receptor was transferred with the lipofectin. Results Microinjection of AS-ONs targeting M5 muscarinic receptor in the ventral tegmental area （VTA） blocked the expression of behavioral sensitization induced by heroin priming in rats. Meanwhile, the expression of FosB-positive neurons in either the NAc or the dentate gyrus （DG） of the hippocam- pus increased in heroin-induced locomotor sensitized rats. The enhancement of FosB-positive neurons in the NAc or DG could be inhibited by microinjection of M5 muscarinic receptor AS-ONs into the VTA before the heroin-induced locomotor sensitization was performed. In contrast, microinjection of M5 muscarinic receptor sense oligonucleotide （S-ONs） into the VTA did not block the expression of behavioral sensitization or the expression of FosB in the NAc or DG in the heroin sensitized rats. Conclusion Blocking M5 muscarinic receptor in the VTA inhibits the expression of heroin-induced locomotor sensitization, which is associated with the regulation of FosB expression in the NAc and hippocampus neurons. M5 muscarinic receptor may be a useful pharmacological target for the treatment of heroin addiction.

线纹海马(Hippocampus erectus)不同养殖密度下水体理化因子和细菌数量的动态变化

研究线纹海马(Hippocampus erectus)在室内水泥池不同养殖密度下,水体环境因子和细菌数量的动态变化情况。结果表明,在一个倒池换水周期中,养殖组1和养殖组2的磷酸磷(PO43--P)、硝酸氮(NO3--N)、亚硝酸氮(NO2--N)和氨氮(NH4+-N)等离子物质的浓度和细菌、弧菌和异养菌数量均随着养殖时间的推移不断上升,通常在换水后9d或12d达到最高,再次换水后降到极低值。单因素方差分析结果表明,在不同养殖密度下,PO43--P、NO3--N、NO2--N和NH4+-N等离子浓度随着养殖密度的升高而升高;而低密度养殖池中细菌数比高密度养殖池的细菌数显著更高。养殖水体中的PO43--P浓度与异养细菌数呈负相关关系,NO2--N浓度与细菌数量和弧菌数呈正相关关系,NO3--N浓度与细菌数、异养菌数和弧菌数呈负相关关系,NH4+-N浓度与细菌数、异养菌数和弧菌数均呈正相关关系。研究结果可为科学开展海马室内规模化养殖提供理论参考。

大海马(Hippocampus kuda Bleeker)幼体口吻部骨骼形态观察及其对摄食的影响

通过对10尾2?3日龄的幼体海马的固定、染色、消化的研究,用显微镜对其摄食器官的构成进行详细观察,明确了幼体海马管状鼻内骨骼的结构。结果显示,幼体海马在摄食时,其舌骨角、后翼骨、方骨、上颌骨、续骨起到支撑等重要的作用;海马幼鱼期续骨与后翼骨之间的夹缝结构,可使略大的饵料通过。因此,可以在养殖过程中通过适当地增加饵料的粒径,有效地提高幼体摄食效率,从而提高存活率。

线纹海马Hippocampus erectus的tlr21基因结构及其对CpG-ODN的应答特征

作为先天性免疫反应中重要的模式识别受体之一,TLR(toll-likereceptor)基因家族介导的先天性免疫是脊椎动物抵御病原微生物的重要防线。研究分析了线纹海马Hippocampus erectus tlr21基因的序列特征,并基于抗原注射实验探讨了海马tlr21的免疫功能。线纹海马tlr21基因的开放阅读框长度为2946bp,编码981个氨基酸,预测其编码蛋白相对分子量为246.98kDa,理论等电点为4.78。tlr21编码蛋白主要包含1个信号肽和3个功能结构域:胞外区具有14个富含亮氨酸重复序列的结构域(LRR),跨膜区具有富含半胱氨酸的结构域,胞内区则具有TIR结构域。同源性比较和系统进化分析表明,线纹海马tlr21基因与虎尾海马Hippocampuscomestlr21基因的同源性最高,其次与斜带石斑鱼Epinephelus coioides、牙鲆Paralichthys olivaceus、大菱鲆Scophthalmus maximus和红鳍东方鲀Takifugu rubripes的tlr21基因聚为一枝。tlr21基因在线纹海马的脑、鳃、肝、肠、肾、性腺、肌肉和育儿袋各组织均有分布,肾脏中表达量最高。抗原注射实验结果发现,线纹海马Tlr21对不同类型CpG寡脱氧核苷酸(CpG-ODNs)的识别能力存在差异,其中,CpG-2007和CpG-HC4040对海马肾脏tlr21的mRNA表达量具有显著的促进作用(P<0.05)。研究表明,线纹海马Tlr21能够通过识别含CpG序列的DNA发挥免疫识别作用,研究结果将有助于系统认识海马免疫系统中TLR家族基因的功能特征,为建立海马病害防治策略提供理论依据。

线纹海马(Hippocampus erectus)性腺特异性结构与生殖细胞发育特征研究

海马属(Hippocampus)鱼类具有独特的雄性育儿繁殖方式,其卵巢和精巢结构也极其独特。本研究系统阐明了线纹海马(Hippocampuserectus)的性腺及生殖细胞的发育特征,根据组织学结构和细胞形态学变化特征,将线纹海马的精巢和卵巢发育过程均分为6个时期。其中,卵巢发育方式为不同步成熟型,Ⅰ期卵巢只包含第Ⅰ时相卵母细胞,包括卵原细胞和早期初级卵母细胞(d<20μm);Ⅱ期卵巢开始出现第Ⅱ时相卵母细胞(d=20~140μm);Ⅲ期卵巢卵母细胞数量显著增多,体积增大,并开始出现第Ⅲ时相卵母细胞(d=140~260μm),此时细胞内开始出现皮质小泡、卵黄颗粒和卵黄膜;Ⅳ期卵巢开始出现第Ⅳ时相卵母细胞(d=260~1100μm),卵黄颗粒充满整个细胞质,形成过渡期的卵黄球;Ⅴ期卵巢出现大量第Ⅴ时相成熟卵母细胞(d=1100~2000μm),细胞内形成流动性卵黄囊;Ⅵ期卵巢为排卵不久后的卵巢,卵母细胞数量显著减少。线纹海马精巢属于非限制型小叶精巢,Ⅰ期精巢主要含精原细胞,核大,含一到多个核仁;Ⅱ期精巢开始形成精小囊,囊内出现初级精母细胞;Ⅲ期精巢呈乳白色,开始出现次级精母细胞;Ⅳ期精巢体积较Ⅲ期时显著增大,开始出现精子细胞,并逐渐移向中央生精腔;Ⅴ期精巢内含大量的成熟精子,随时准备释放。精子释放后精巢进入Ⅵ期,残留少量精细胞在生精腔中。组织化学反应结果显示,氨基酸、蛋白质和脂肪的信号在卵母细胞的细胞质、卵黄囊中呈阳性,且随着卵母细胞的发育而增强。本研究结果为进一步探索海马属鱼类雄性繁殖策略提供了重要的基础数据。

Relationship between Cognition Function and Hippocampus Structure after Long-term Microwave Exposure

Objective To analyze the effects of long-term microwave exposure on hippocampal structure and function in the rat.Methods Experiments were performed on 184 male Wistar rats（three exposure groups and a sham group）.Microwaves were applied daily for 6 min over 1 month at average power densities of 2.5,5,and 10 mW/cm2.Learning and memory abilities were assessed by Morris water maze.High performance liquid chromatography was used to detect neurotransmitter concentrations in the hippocampus.Hippocampal structures were observed by histopathological analysis.Results Following long-term microwave exposure there was a significant decrease in learning and memory activity in the 7 d,14 d,and 1 m in all three microwave exposure groups.Neurotransmitter concentrations of four amino acids（glutamate,aspartic acid,glycine,and gamma-aminobutyric acid） in hippocampus were increased in the 2.5 and 5 mW/cm2 groups and decreased in the 10 mW/cm2 group.There was evidence of neuronal degeneration and enlarged perivascular spaces in the hippocampus in the microwave exposure groups.Further,mitochondria became swollen and cristae were disordered.The rough endoplasmic reticulum exhibited sacculated distension and there was a decrease in the quantity of synaptic vesicles.Conclusion These data suggest that the hippocampus can be injured by long-term microwave exposure,which might result in impairment of cognitive function due to neurotransmitter disruption.

Microwave Exposure Impairs Synaptic Plasticity in the Rat Hippocampus and PC12 Cells through Over-activation of the NMDA Receptor Signaling Pathway

Objective The aim of this study is to investigate whether microwave exposure would affect the N-methyI-D-aspartate receptor （NMDAR） signaling pathway to establish whether this plays a role in synaptic plasticity impairment. Methods 48 male Wistar rats were exposed to 30 mW/cm^2 microwave for 10 min every other day for three times. Hippocampal structure was observed through H＆E staining and transmission electron microscope. PC12 cells were exposed to 30 mW/cm^2 microwave for 5 min and the synapse morphology was visualized with scanning electron microscope and atomic force microscope. The release of amino acid neurotransmitters and calcium influx were detected. The expressions of several key NMDAR signaling molecules were evaluated. Results Microwave exposure caused injury in rat hippocampal structure and PC12 cells, especially the structure and quantity of synapses. The ratio of glutamic acid and gamma-aminobutyric acid neurotransmitters was increased and the intracellular calcium level was elevated in PC12 cells. A significant change in NMDAR subunits （NR1, NR2A, and NR2B） and related signaling molecules （CaZ＋/calmodulin-dependent kinase II gamma and phosphorylated cAMP-response element binding protein） were examined. Conclusion 30 mW/cm^2 microwave exposure resulted in alterations of synaptic structure, amino acid neurotransmitter release and calcium influx. NMDAR signaling molecules were closely associated with impaired synaptic plasticity.

Behavioral Abnormality along with NMDAR-related CREB Suppression in Rat Hippocampus after Shortwave Exposure

Objective To estimate the detrimental effects of shortwave exposure on rat hippocampal structure and function and explore the underlying mechanisms. Methods One hundred Wistar rats were randomly divided into four groups(25 rats per group) and exposed to 27 MHz continuous shortwave at a power density of 5, 10, or 30 m W/cm^2 for 6 min once only or underwent sham exposure for the control. The spatial learning and memory, electroencephalogram(EEG), hippocampal structure and Nissl bodies were analysed. Furthermore, the expressions of N-methyl-D-aspartate receptor(NMDAR) subunits(NR1, NR2 A, and NR2 B), c AMP responsive element-binding protein(CREB) and phosphorylated CREB(p-CREB) in hippocampal tissue were analysed on 1, 7, and 14 days after exposure. Results The rats in the 10 and 30 m W/cm^2 groups had poor learning and memory, disrupted EEG oscillations, and injured hippocampal structures, including hippocampal neurons degeneration, mitochondria cavitation and blood capillaries swelling. The Nissl body content was also reduced in the exposure groups. Moreover, the hippocampal tissue in the 30 m W/cm^2 group had increased expressions of NR2 A and NR2 B and decreased levels of CREB and p-CREB. Conclusion Shortwave exposure(27 MHz, with an average power density of 10 and 30 m W/cm^2) impaired rats' spatial learning and memory and caused a series of dose-dependent pathophysiological changes. Moreover, NMDAR-related CREB pathway suppression might be involved in shortwave-induced structural and functional impairments in the rat hippocampus.

Ulinastatin suppresses endoplasmic reticulum stress and apoptosis in the hippocampus of rats with acute paraquat poisoning

Lung injury is the main manifestation of paraquat poisoning. Few studies have addressed brain damage after paraquat poisoning. Ulinastatin is a protease inhibitor that can effectively stabilize lysosomal membranes, prevent cell damage, and reduce the production of free radicals. This study assumed that ulinastatin would exert these effects on brain tissues that had been poisoned with paraquat. Rat models of paraquat poisoning were intraperitoneally injected with ulinastatin. Simultaneously, rats in the control group were administered normal saline. Hematoxylin-eosin staining showed that most hippocampal cells were contracted and nucleoli had disappeared in the paraquat group. Fewer cells in the hippocampus were concentrated and nucleoli had dis- appeared in the ulinastatin group. Western blot assay showed that expressions of GRP78 and cleaved-caspase-3 were significantly lower in the ulinastatin group than in the paraquat group. Immunohistochemical findings showed that CHOP immunoreactivity was significantly lower in the ulinastatin group than in the paraquat group. Terminal deoxynucleotidyl transferase-medi- ated dUTP nick end labeling staining showed that the number of apoptotic cells was reduced in the paraquat and ulinastatin groups. These data confirmed that endoplasmic reticular stress can be induced by acute paraqnat poisoning. Ulinastatin can effectively inhibit this stress as well as cell apoptosis, thereby exerting a neuroprotective effect.

Study of the hippocampus and the anterior cingulate gyrus by proton MR spectroscopy in patients with post-traumatic stress disorder

Objective:To explore the characteristics of metabolic changes in patients with post-traumatic stress disorder through 1H-MRS in neuroanatomical circuit comparing with age-matches controls.Methods:Fifty patients with post-traumatic stress disorder and SO gender-and agematched normal controls were involved.The neurochemical abnormalities including the levels of choline(Cho)/ creatine(Cr) and N-acetylaspartate(NAA)/Cr were measured respectively in hippocampus and the anterior cingulate gyrus with three-dimension 1H-proton specrroscopy(3D 1H-MRS).Results:The values of NAA/Cr ratios in hippocampus and the anterior cingulate gyrus were significant lower in patients with post-traumatic stress disorder(1.71±0.32,left l.58±0.29, right 1.55±0.31) than that in controls(2.24±0.41,left 1.98±0.27,right 2.02±0.36)(P【0.05).but the values of Cho/Cr in hippocampus(left 1.64±0.23,right 1.66±0.34) were no significant with that of controls(left 1.48±0.29,right 1.54±0.38).Values of Cho/Cr in cingulate gyrus were significant higher in post-traumatic stress disorder patients(I.88±0.44) than that in controls(1.37.±0.32) (P【0.05).Conclusions:The results indicate some special neurochemical and histological structure changes in post-traumatic stress disorder patients,which might occurre earlier in anterior cingulate gyrusthe than in hippocampus.