Progesterone treatment before experimental hypoxia-ischemia enhances the expression of glucose transporter proteins GLUT1 and GLUT3 in neonatal rats

Progesterone is an efficient candidate for treating stroke and traumatic brain damage. The current study was designed to investigate the effects of progesterone on glucose transporter proteins (GLUT1 and GLUT3) during hypoxic-ischemic injury in a neonatal rat model. We demonstrated strong staining for GLUT1 in the walls of blood vessels and GLUT3 immunoreactivity in hippocampal neurons after hypoxiaischemia. Hypoxia-ischemia elevated GLUT1 and GLUT3 at both the mRNA and protein levels in the hippocampus, and pre-treatment with progesterone (8 mg/kg) further enhanced their accumulation until 24 h after hypoxic-ischemic injury. These results showed that progesterone treatment induced the accumulation of both GLUT1 and GLUT3 transporters, and an energy-compensation mechanism may be involved in the neuroprotective effect of progesterone during hypoxic-ischemic injury after cerebral ischemic attacks.     

A case-control association study of <Emphasis Type="Italic">NRXN1</Emphasis> polymorphisms with schizophrenia in Chinese Han population

Background  

Recent research has implicated that mutations in the neurexin-1 (NRXN1) gene on chromosome 2p16.3 might play a role in schizophrenia, autism, and nicotine dependence. In order to explore the association of NRXN1 polymorphisms with schizophrenia, we made a case-control association study in Chinese Han population.     

癫痫大鼠模型的视频脑电图研究

目的探讨癫痫大鼠模型的视频脑电图检测方法,为评价癫痫大鼠模型寻找实验室依据。方法构建氯化锂和匹罗卡品急性癫痫大鼠模型,利用视频脑电监测仪观察脑电图动态变化过程。结果大鼠腹腔未注射氯化锂和匹罗卡品药物前脑电图各个导联均表现为9～12 Hz的α波或17～19 Hz的β波,波幅20～80μV,即基础波。未观察到棘波、尖波等癫痫样波。注入氯化锂和匹罗卡品后平均5～80 min中央区出现散在的尖波、棘波为先兆期,然后逐渐波及到各个导联,可见棘波、尖波及短程放电,强直-阵挛期表现为棘波、尖波、多棘-慢波及棘慢波长程放电。结论视频脑电图可作为评价癫痫大鼠模型有效的检测手段。     

孕期注射Poly（I∶C）对大鼠子代认知行为及脑髓鞘碱性蛋白的影响

目的 通过分析孕鼠感染多聚肌苷酸：多聚胞苷酸（Polyriboinosinic-polyribocytidilic acid,Poly （I∶C）后子代行为学和脑白质髓鞘碱性蛋白（myelin basic protein,MBP）的变化,了解脑白质在孕期感染所致子代行为异常中的作用.方法两组模型组孕鼠分别给予5 mg/kg Poly（I∶C）和10 mg/kgPoly（I∶C）处理,对照组给予5 mg/kg生理盐水处理.待子代生长至8周时用前脉冲抑制实验、被动规避实验、主动规避实验检测子代精神分裂症样行为,用免疫组化方法观察脑白质MBP的变化.结果 前脉冲抑制结果显示PP2、PP4、PP8差异有显著性（F=10.381,P=0.001,F=10.313,P=0.001,F=15.233,P=0.000）,两个模型组均小于对照组,双倍剂量组均小于单倍剂量组（P＜0.05）;被动规避结果显示T1、T2差异有显著性（F=17.524,P=0.000,F=23.555,P=0.000）,两个模型组的T1时间均大于对照组,双倍剂量组大于单倍剂量组（P＜0.05）;两模型组T2时间均小于对照组,双倍剂量组小于单倍剂量组（P＜0.05）;主动规避结果显示总条件反射次数和条件反射率差异有显著性（F=8.631,P=0.000,F=6.986,P=0.001）,两个模型组均小于对照组,双倍剂量组小于单倍剂量组（P＜0.05）;两模型组大鼠脑白质MBP免疫组化结果与对照组相比有统计学意义（P＜0.05）,两模型组比较差异无统计学意义（P＞0.05）.结论 Poly（I∶C）处理后子鼠存在行为学和MBP的改变,且行为学改变的程度与药物剂量有相关性.     

卒中后抑郁与炎症因子的关系研究

目的分析卒中后抑郁(post-stroke depression,PSD)大鼠血清IL-17A水平、海马IL-1β、TNF-α mRNA表达的变化,探讨PSD的病理生理机制。方法将30只成年的无特定病原体级SD雄性大鼠随机分为假手术组、卒中组、PSD组,对各组大鼠进行基线行为学评估,其中卒中组和PSD组大鼠行大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)缺血再灌注处理,1周后对PSD组大鼠行慢性轻度刺激(chronic unpredictable mild stress,CUMS),每天给予1~2种刺激,连续4周,CUMS刺激4周后对各组大鼠进行行为学评估。评估结束后采用尼氏染色观察各组大鼠海马区神经元形态,使用ELISA方法检测大鼠血清中IL-17A水平,实时荧光定量PCR检测大鼠海马IL-1β、TNF-α mRNA表达。观察PSD情况下,血清及海马神经元炎症因子的表达水平及海马损伤情况。结果假手术组、卒中组和PSD组大鼠血清的IL-17A水平分别为18.56±2.56 pg/mL、40.78±4.13 pg/mL和52.10±5.22 pg/mL,三组比较差异有统计学意义;假手术组、卒中组、PSD组大鼠海马区IL-1βmRNA相对表达水平分别为0.570±0.322、2.617±0.128和3.189±0.107,三组比较差异有统计学意义;假手术组、卒中组、PSD组大鼠海马区TNF-α mRNA基因相对表达水平分别为0.999±0.007、1.258±0.042和1.623±0.041,三组比较差异有统计学意义;尼氏染色提示卒中组、PSD组海马区CA1区神经元存在损伤,以PSD组最明显。结论 PSD组大鼠血清IL-17A水平上调,海马IL-1β、TNF-αmRNA高表达,提示PSD发生的病理生理机制中可能有炎症反应参与。     

Statistical shape analysis using 3D Poisson equation—A quantitatively validated approach

Statistical shape analysis has been an important area of research with applications in biology, anatomy, neuroscience, agriculture, paleontology, etc. Unfortunately, the proposed methods are rarely quantitatively evaluated, and as shown in recent studies, when they are evaluated, significant discrepancies exist in their outputs. In this work, we concentrate on the problem of finding the consistent location of deformation between two population of shapes. We propose a new shape analysis algorithm along with a framework to perform a quantitative evaluation of its performance. Specifically, the algorithm constructs a Signed Poisson Map (SPoM) by solving two Poisson equations on the volumetric shapes of arbitrary topology, and statistical analysis is then carried out on the SPoMs. The method is quantitatively evaluated on synthetic shapes and applied on real shape data sets in brain structures.     

Association study of RELN polymorphisms with schizophrenia in Han Chinese population

Schizophrenia (SZ) is a common and complex psychiatric disorder with a strong genetic component. Previous research suggests that mutations altering genes in neurodevelopmental pathways contribute to SZ. Reelin gene (RELN) maps to chromosome 7q22.1, the encoded protein plays a pivotal role in guiding neuronal migration, lamination and connection during embryonic brain development. Several reports had indicated that reduced RELN expression is associated with human mental illnesses such as SZ, mood disorders and autism. In this study, case-control association analyses were performed in the Han Chinese population to determine if the RELN gene is a susceptibility gene for SZ. Thirty-seven single nucleotide polymorphisms (SNPs) were genotyped in 528 paranoid SZ patients and 528 control subjects. A significant association was found between rs12705169 and SZ (p = 0.001). Moreover, the haplotypes constructed from five SNPs showed significant differences between cases and controls (p = 0.041). When subjects were divided by gender, rs12705169 remained significant difference only in females (OR = 0.24, 95%CI = 0.14-0.40 for CC and OR = 0.40, 95%CI = 0.27-0.58 for AC), both in the allele and genotype (p = 0.0001 for both). This study describes a positive association between RELN and SZ in the Han Chinese population, and provides genetic evidence to support the gender difference of SZ.     

慢性吗啡依赖大鼠条件性位置厌恶模型脑腹侧被盖区蛋白激酶A的表达变化

目的分析慢性吗啡依赖大鼠条件性位置厌恶(conditioned place aversion,CPA)模型脑腹侧被盖区(ventraltegmental area,VTA)蛋白激酶A(protein kinase A,PKA)蛋白表达的适应性变化,探讨阿片依赖戒断后厌恶动机形成的生物学基础。方法①将72只雄性Sprague-Dawley(SD)大鼠分为研究组(慢性吗啡注射+纳洛酮催瘾组,MN组),对照组(慢性吗啡注射+生理盐水组,MS组;慢性生理盐水注射+纳洛酮组,SN组),每组24只。采用慢性吗啡腹腔注射(10mg/kg,Bid,ip.)后予1次纳洛酮(0.3mg/kg)催瘾注射,同时与条件性位置训练箱搭配使用建立大鼠CPA模型。②在CPA建立前后,采用免疫组织化学方法检测VTA内PKA蛋白表达情况。结果 CPA建立前,MN组PKA蛋白表达水平与对照组(MS组和SN组)比较差异无统计学意义(F=0.013,P=0.987)。CPA建立后,3组PKA蛋白表达水平比较差异有统计学意义(F=9.853,P=0.018),MN组灰度值(127.500±3.536)显著低于MS组[(140.500±3.697),P<0.05]和SN组[(138.000±2.944),P<0.05]。结论①VTA内PKA蛋白高表达,可能是CPA建立的神经机制之一。②VTA内PKA的适应性变化可能是物质依赖戒断后CPA相关神经可塑性变化的重要分子基础之一。