N—甲基天冬氨酸受体拮抗剂AP—5在海马对兔P3波电位的 …

目的 推测Ｎ－甲基天冬氨酸受体（Ｎ－ｍｅｔｈｙｌ－Ｄ－ａｓｐａｒａｔｅ ｒｅｃｅｐｔｏｒ,ＮＭＤＡＲ）的兴奋性突触后电位（ｅｘｃｉｔａｔｏｒｙ ｐｏｓｔｓｙｎａｐｔｉｃ ｐｏｔｅｎｔｉａｌｓ,ＥＰＳＰ）活动对兔Ｐ３波的作用。方法 采用ＮＭＤＡＲ竞争性拮抗剂ＡＰ－５（３．１２５,６．２５,１２．５ｍｍｏｌ／Ｌ）在海马ＣＡ１,ＣＡ３微量注入,观察Ｐ３波电位变化。     

关于医学名词英文缩写的启事

ＡＣＴＨ促肾上腺皮质激素Ａ／Ｇ白蛋白／球蛋白比值ＡＬＴ丙氨酸转氨酶ＡＳＴ天冬氨酸转氨酶Ｃｃｒ肌酐清除率ＣＯＰＤ慢性阻塞性肺疾病ＣＴ计算机Ｘ线体层扫描ＤＩＣ弥散性血管内凝血ＤＮＡ脱氧核糖核酸ＨＢｃＡｂ乙型肝炎核心抗体ＨＢｅＡｂ乙型肝炎ｅ抗体ＨＢｅＡｇ乙型肝炎ｅ抗原ＨＢｓＡｂ乙型肝炎表面抗体ＨＢｓＡｇ乙型肝炎表面抗原ＨＤＬＣ高密度脂蛋白胆固醇Ｉｇ免疫球蛋白ＬＤＬＣ低密度脂蛋白胆固醇ＭｃＡｂ单克隆抗体ＯＴ旧结核菌素试验ＰＣＲ聚合酶链反应ＰＥＴ正电子发射断层扫描ＲＦ类风湿因子ＳＬＥ系统性红斑狼疮ＳＰ…     

MOTSA 和MTC MRA 对脑动静脉畸形的诊断价值

目的 分析脑ＡＶＭ的３Ｄ－ＴＯＦ ＭＲＡ结合ＭＯＴＳＡ（ｍｕｌｔｉｐｌｅ ｏｖｅｒｌａｐｐｉｎｇ ｔｈｉｎ ｓｌａｂ ａｃｑｕｉｓｉｔｉｏｎ）和ＭＴＣ（ｍａｇｎｅｔｉｚａｔｉｏｎ ｔｒａｎｓｆｅｒ ｃｏｎｔｒａｓｔ）的表现。探讨其诊断价值。方法 使用ＧＥｓｉｇｎａ ｅｃｈｏ ｓｐｅｅｄ １．５Ｔ超导ＭＲ机对１２０例ＡＶＭ患者分别行ＳＥ序列ＭＲＩ,３Ｄ－ＴＯＦＭＲＡ结合ＭＯＴＳＡ和ＭＴＣ检查。结果     

一种新的NADH-细胞色素b5还原酶基因点突变

目的　为了查明中国人遗传性高铁血红蛋白血症（ＲＣＭ） 患者的ＮＡＤＨ细胞色素ｂ５ 还原酶（ｂ５Ｒ） 基因突变类型,探讨ＲＣＭ 发生的分子机制。方法　从已报道的１ 例ＲＣＭⅠ型患者的外周血白细胞中提取ＲＮＡ,应用逆转录聚合酶链反应法（ＲＴＰＣＲ） 扩增了ｂ５ＲｃＤＮＡ（９２１ ｂｐ）,测定其ｂ５ＲｃＤＮＡ的全部编码序列。结果　ｂ５ＲｃＤＮＡ基因的第２０３ 位密码子存在（ＴＧＣ→ＴＡＣ）Ｃｙｓ→Ｔｙｒ 的错义突变。经基因组ＰＣＲ限制性片段长度多态性（ＲＦＬＰ） 分析证实该突变并非ＰＣＲ过程中的错配。结论　Ｃｙｓ２０３ →Ｔｙｒ 是ＲＣＭ 的一种新的基因突变类型     

caspase 3在细胞因子调节急性白血病细胞凋亡中的变化

目的 研究ｃａｓｐａｓｅ３在粒细胞集落刺激因子（Ｃ－ＣＳＦ）和粒巨洚细胞集落因子（ＧＭ－ＣＳＦ）调节白血病细胞系ＮＢ４细胞凋亡过程中的变化及其意义。方法 利用细胞这、流式细胞仪分析及ＤＮＡ片段化比率测定,检测Ｇ－ＣＳＦ及ＤＭ－ＣＳＦ对ＮＢ４细胞凋亡的影响,应用荧光分光光度法检测ｃａｓｐａｓｅ３活性变化,并利用ＡＥ－ＤＥＶＤ－ＣＲＯ进行ｃａｓｐａｓｅ３抑制试验。结果 Ｇ－ＣＳＦ能诱导ＮＢ４细胞凋亡,     

关于医学名词英文缩写的启事

ＡＣＴＨ促肾上腺皮质激素Ａ／Ｇ白蛋白／球蛋白比值ＡＬＴ丙氨酸转氨酶ＡＳＴ天冬氨酸转氨酶Ｃｃｒ肌酐清除率ＣＯＰＤ慢性阻塞性肺疾病ＣＴ计算机Ｘ线体层扫描ＤＩＣ弥散性血管内凝血ＤＮＡ脱氧核糖核酸ＨＢｃＡｂ乙型肝炎核心抗体ＨＢｅＡｂ乙型肝炎ｅ抗体ＨＢｅＡｇ乙型肝炎ｅ抗原ＨＢｓＡｂ乙型肝炎表面抗体ＨＢｓＡｇ乙型肝炎表面抗原ＨＤＬＣ高密度脂蛋白胆固醇Ｉｇ免疫球蛋白ＬＤＬＣ低密度脂蛋白胆固醇ＭｃＡｂ单克隆抗体ＯＴ旧结核菌素试验ＰＣＲ聚合酶链反应ＰＥＴ正电子发射断层扫描ＲＦ类风湿因子ＳＬＥ系统性红斑狼疮ＳＰＥＣ…     

关于医学名词英文缩写的启事

ＡＣＴＨ促肾上腺皮质激素Ａ／Ｇ白蛋白／球蛋白比值ＡＬＴ丙氨酸转氨酶ＡＳＴ天冬氨酸转氨酶Ｃｃｒ肌酐清除率ＣＯＰＤ慢性阻塞性肺疾病ＣＴ计算机Ｘ线体层扫描ＤＩＣ弥散性血管内凝血ＤＮＡ脱氧核糖核酸ＨＢｃＡｂ乙型肝炎核心抗体ＨＢｅＡｂ乙型肝炎ｅ抗体ＨＢｅＡｇ乙型肝炎ｅ抗原ＨＢｓＡｂ乙型肝炎表面抗体ＨＢｓＡｇ乙型肝炎表面抗原ＨＤＬＣ高密度脂蛋白胆固醇Ｉｇ免疫球蛋白ＬＤＬＣ低密度脂蛋白胆固醇ＭｃＡｂ单克隆抗体ＯＴ旧结核菌素试验ＰＣＲ聚合酶链反应ＰＥＴ正电子发射断层扫描ＲＦ类风湿因子ＳＬＥ系统性红斑狼疮ＳＰＥＣ…     

阿莫西林胶囊致剥脱性皮炎1例

阿莫西林胶囊致剥脱性皮炎１例ＡＣａｓｅｏｆＥｘｆｏｌｉａｔｉｖｅＤｅｒｍａｔｉｔｉｓＣａｕｓｅｄｂｙＡｍｏｘｉｃｉｌｉｎＣａｐｓｕｌｅ施雁ＳｈｉＹａｎ（ＡｆｉｌｉａｔｅｄＲａｉｌｗａｙＨｏｓｐｉｔａｌｏｆＳｈａｎｇｈａｉＲａｉｌｗａｙＭｅｄｉｃａｌ...     

共焦镜同时检测细胞内Ca2+和pH的变化

目的细胞内游离Ｃａ２＋与胞浆的ｐＨ在不同因素作用下可以改变。研究可以同时检测游离Ｃａ２＋与ｐＨ变化的方法激光扫描共聚焦显微镜观察。方法用胞内游离Ｃａ２＋和ｐＨ荧光探针ｆｌｕｏ３／ＡＭ和ＳＮＡＲＦ１／ＡＭ标记小鼠腹腔巨噬细胞后，在激光扫描共聚焦显微镜（ＡＣＡＳ５７０）下，同时用最适发射波长分别为５３０ｎｍ和大于６０５ｎｍ的检测器１和检测器２检测巨噬细胞内ｆｌｕｏ３／ＡＭ和ＳＮＡＲＦ１／ＡＭ的荧光强度变化。结果检测器１和检测器２分别只检测反映细胞内游离Ｃａ２＋和ｐＨ变化的ｆｌｕｏ３／ＡＭ和ＳＮＡＲＦ１／ＡＭ所发荧光的变化；ＳＮＡＲＦ１／ＡＭ和ｆｌｕｏ３／ＡＭ所发荧光相互不影响。结论激光扫描共聚焦显微镜可同时检测细胞内游离Ｃａ２＋和ｐＨ的变化。     

5%孟氏液保留灌肠致休克1例

５％孟氏液保留灌肠致休克１例ＡＣａｓｅＲｅｐｏｒｔｏｆＳｈｏｃｋＣａｕｓｅｄｂｙＲｅｔｅｎｔｉｏｎＥｎｅｍａｏｆ５％ＭｏｎｎｅｌＳｏｌｕｔｉｏｎ郑茹云①ＺｈｅｎｇＲｕｙｕｎ（Ｐｅｏｐｌｅ’ｓＨｏｓｐｉｔａｌｏｆＳｕｉｃｈａｎｇＣｏｕｎｔｙ，Ｚｈｅｊ...     

Expression pattern of NMDA receptors reveals antiepileptic potential of apigenin 8-C-glucoside and chlorogenic acid in pilocarpine induced epileptic mice

The present study was aimed to evaluate the effect of apigenin 8-C-glucoside (Vitexin) and chlorogenic acid on epileptic mice induced by pilocarpine and explored its possible mechanisms. Intraperitonial administration of pilocarpine (85 mg/kg) induced seizure in mice was assessed by behavior observations, which is significantly (p > 0.05) reduced by apigenin 8-C-glucoside (AP8CG) (10 mg/kg) and chlorogenic acid (CA) (5 mg/kg), similar to diazepam. Seizure was accompanied by an imbalance in the levels of Gamma-aminobutyric acid (GABA) and glutamate in the pilocarpine administered group. Moreover, convulsion along with reduced acetylcholinesterase, increased monoamine oxidase and oxidative stress was observed in epileptic mice brain. AP8CG and CA significantly restored back to normal levels even at lower doses. Further, increased lipid peroxidation and nitrite content was also significantly attenuated by AP8CG and CA. However, CA was found to be more effective when compared to AP8CG. In addition, the mRNA expression of N-methyl-d-aspartate receptor (NMDAR), mGluR1 and mGlu5 was significantly (P ≤ 0.05) inhibited by AP8CG and CA in a lower dose. The mRNA expression of GRIK1 did not differ significantly in any of the group and showed a similar pattern of expression. Our result shows that AP8CG and CA selectively inhibit NMDAR, mGluR1 and mGlu5 expression. Modification in the provoked NMDAR calcium response coupled with neuronal death. Hence, these findings underline that the polyphenolics, AP8CG and CA have exerted antiepileptic and neuroprotective activity by suppressing glutamate receptors.     

The hypotensive action of rilmenidine is dependent on functional N-methyl-D-aspartate receptor in the rostral ventrolateral medulla of conscious spontaneously hypertensive rats

Rilmenidine is a second-generation centrally acting antihypertensive drug that acts mainly through the activation of the imidazoline (I(1)) receptor in the rostral ventrolateral medulla (RVLM). To investigate the contribution of the N-methyl-D-aspartate receptor (NMDAR) to the hypotensive action of rilmenidine, experiments were undertaken in conscious male spontaneously hypertensive rats (SHRs). Microinjection of cumulative doses of rilmenidine (10, 20, and 40 nmol) at 10- to 15-min intervals, into the RVLM elicited dose-dependent hypotensive and bradycardic response. Pretreatment with intra-RVLM 2-amino-5-phosphonopentanoic acid (AP5) (2 nmol), a selective NMDAR antagonist, not only abolished the hypotensive response elicited by intra-RVLM rilmenidine (40 nmol) but also converted it to a pressor response (-24 +/- 1 versus 17 +/- 7 mm Hg; P < 0.05) and significantly attenuated the bradycardic response (-72 +/- 18 versus -24 +/- 20 bpm; P < 0.05). The blood pressure response to intra-RVLM N-methyl-D-aspartate (NMDA) depended on the dose applied. Whereas intra-RVLM NMDA (>20 pmol) produced the expected pressor response, a lower dose (10 pmol) reduced mean arterial pressure (MAP) (-14 +/- 3 mm Hg) and heart rate (-21 +/- 12 bpm). The divergent MAP responses were attenuated by intra-RVLM AP5 (2 nmol), which implicates the NMDAR in the pressor as well as the depressor response. The present findings suggest that the NMDAR in the RVLM of the SHR 1) exerts dual effects on blood pressure, with the response type depending on the level of NMDAR activation, and 2) plays a pivotal role in the hypotension mediated by I(1) receptor activation in the RVLM.     

Down-regulation of synaptic GluN2B subunit-containing N-methyl-D-aspartate receptors: a physiological brake on CA1 neuron α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid hyperexcitability during benzodiazepine withdrawal

A significant link was previously established between benzodiazepine withdrawal anxiety and a progressive increase in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) potentiation in hippocampal CA1 neurons from rats withdrawn up to 2 days from 1-week oral administration of the benzodiazepine flurazepam (FZP). Despite AMPAR current potentiation, withdrawal anxiety was masked by a 2-fold reduction in CA1 neuron N-methyl-D-aspartate receptor (NMDAR) currents since preinjection of an NMDA antagonist restored NMDAR currents and unmasked anxiety in 2-day FZP-withdrawn rats. In the current study, GluN subunit levels in postsynaptic density (PSD)-enriched subfractions of CA1 minislices were compared with GluN2B-mediated whole-cell currents evoked in CA1 neurons in hippocampal slices from 1- and 2-day FZP-withdrawn rats. GluN1 and GluN2B, although not the phosphoSer1303-GluN2B ratio or GluN2A subunit levels, were decreased in PSD subfractions from 2-day, but not 1-day, FZP-withdrawn rats. Consistent with immunoblot analyses, GluN2B-mediated NMDAR currents evoked in slices from 2-day FZP-withdrawn rats were decreased in the absence, but not the presence, of the GluN2B subunit-selective antagonist ifenprodil. In contrast, ifenprodil-sensitive NMDAR currents were unchanged in slices from 1-day withdrawn rats. Because AMPA (1 μM) preincubation of slices from 1-day FZP-withdrawn rats induced depression of GluN2B subunit-mediated currents, depression of NMDAR currents was probably secondary to AMPAR potentiation. CA1 neuron NMDAR currents were depressed ～50% after 2-day withdrawal and offset potentiation of AMPAR-mediated currents, leaving total charge transfer unchanged between groups. Collectively, these findings suggest that a reduction of GluN2B-containing NMDAR may serve as a homeostatic feedback mechanism to modulate glutamatergic synaptic strength during FZP withdrawal to alleviate benzodiazepine withdrawal symptoms.     

电针对大鼠海马兴奋性突触后电位长时程增强的作用

背景海马长时程增强(1ong-term potentiation,LTP)与行为学研究相结合,已被广泛用于包括中医药在内的改善学习记忆功能和治疗老年性痴呆的研究.目的观察电针对麻醉状态下正常和东莨菪碱引起的学习记忆减退模型大鼠海马兴奋性突触后电位(excitatory postsynaptic potential,EPSP)LTP的作用.设计随机对照研究.地点和材料SD大鼠40只,体质量270～310 g,单纯随机分成为对照组、电针组、模型组和模型+电针治疗组,每组10只.干预引导大鼠海马齿状回颗粒细胞层突触后兴奋性电位群(EPSPs),强直刺激大脑皮质前穿质区引起海马突触LTP反应;用东莨菪碱制备学习记忆障碍模型;电针(疏密波3～5 mA,30 min)大椎和双侧肾俞穴;观察电针对正常和模型大鼠海马LTP的影响.主要观察指标强直刺激前和强直刺激诱发后0,60,120 min LTP群发电位信号(PS),PS的EPSP潜伏期,PS锋值潜伏期,EPSP的斜率,PS锋值和PS锋面积(PSa).结果①电针对强直刺激诱发的海马突触LTP效应的作用强于对照组.与对照组比,EPSP潜伏期明显缩短[相对于强直刺激前的变化率对照组与电针组分别为(-7.8±2.6)%比(-14.4±7.7)%,差异有显著性意义(t=2.568 1,P＜0.05)];EPSP的斜率增加(t=2.436 4,P＜0.05);PS锋面积增大(t=2.750 8～2.990 9,P＜0.05),且维持时间长于对照组.②东莨菪碱可显著抑制强直刺激诱发的海马突触LTP,表现为EPSP潜伏期和PS锋值潜伏期延长,与对照组比较差异均有非常显著性意义(t=4.564 8～5,996 5,P均＜0.01);EPSP的斜率下降,PS锋值和PS锋面积变小.③电针能显着对抗东莨菪碱对海马突触LTP的抑制作用,与模型组比较各参数均有统计学意义.结论电针对强直刺激引起的海马突触LTP有一定的易化作用,并对东莨菪碱引起的学习记忆障碍有显著的对抗作用.     

Regulation of Hippocampal and Behavioral Excitability by Cyclin-Dependent Kinase 5

Cyclin-dependent kinase 5 (Cdk5) is a proline-directed serine/threonine kinase that has been implicated in learning, synaptic plasticity, neurotransmission, and numerous neurological disorders. We previously showed that conditional loss of Cdk5 in adult mice enhanced hippocampal learning and plasticity via modulation of calpain-mediated N-methyl-D-aspartic acid receptor (NMDAR) degradation. In the present study, we characterize the enhanced synaptic plasticity and examine the effects of long-term Cdk5 loss on hippocampal excitability in adult mice. Field excitatory post-synaptic potentials (fEPSPs) from the Schaffer collateral CA1 subregion of the hippocampus (SC/CA1) reveal that loss of Cdk5 altered theta burst topography and enhanced post-tetanic potentiation. Since Cdk5 governs NMDAR NR2B subunit levels, we investigated the effects of long-term Cdk5 knockout on hippocampal neuronal excitability by measuring NMDAR-mediated fEPSP magnitudes and population-spike thresholds. Long-term loss of Cdk5 led to increased Mg²⁺-sensitive potentials and a lower threshold for epileptiform activity and seizures. Biochemical analyses were performed to better understand the role of Cdk5 in seizures. Induced-seizures in wild-type animals led to elevated amounts of p25, the Cdk5-activating cofactor. Long-term, but not acute, loss of Cdk5 led to decreased p25 levels, suggesting that Cdk5/p25 may be activated as a homeostatic mechanism to attenuate epileptiform activity. These findings indicate that Cdk5 regulates synaptic plasticity, controls neuronal and behavioral stimulus-induced excitability and may be a novel pharmacological target for cognitive and anticonvulsant therapies.     

移植脑源性神经营养因子转染的骨髓间充质干细胞对AD大鼠的影响

目的:研究移植脑源性神经营养因子(BDNF)转染的骨髓间充质干细胞(MSCs)对阿尔茨海默病(AD)大鼠N-甲基-D-天冬氨酸受体1(NMDAR1)及认知功能的影响。方法:将50只SD大鼠随机平均分为正常对照组、假手术组、AD组、MSCs组、BDNF组。正常对照组不予任何处理,其他4组制备AD模型;MSCs组和BDNF组于制模第11天分别注入10μL(约5×106)MSCs或pIRESneo-EGFP-BDNF转染的MSCs。采用Morris水迷宫测试大鼠学习记忆能力,免疫组化染色法测定NMDAR1水平。结果:MSCs组、BDNF组与AD组比较平均逃避潜伏期(AEL)明显缩短、跨平台次数显著增加;BDNF组较MSCs组改善更显著(P<0.01),NMDAR1水平更高(P<0.01)。结论:BDNF转染骨髓MSCs对AD大鼠的认知有改善作用,且促进海马区NMDAR1的表达。     

Mu opioid receptor activation reduces inhibitory postsynaptic potentials in hippocampal CA3 pyramidal cells of rat and guinea pig

Using intracellular recording techniques, we characterized synaptic responses of CA3 pyramidal cells to mu and kappa agonists in hippocampal slices from rats and guinea pigs. In rat CA3 pyramidal cells, the mu selective agonist (N-MePhe3,D-Pro4)-morphiceptin (PLO17) inhibited both the early and the late inhibitory postsynaptic potentials (IPSPs) and increased excitatory postsynaptic potential (EPSP) amplitudes. Voltage clamp analysis of synaptic currents indicated that the excitatory postsynaptic current were not increased by PLO17, showing that the apparent increase in EPSPs was a result of a decrease in the underlying IPSP. The kappa agonists trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate and dynorphin A (1-17) had no effect on EPSPs or IPSP conductances measured in rat pyramidal cells. Maximal inhibition of IPSPs by PLO17 resulted in a bursting response to stimulation in rat but not guinea pig CA3 pyramidal cells. In guinea pig CA3 pyramidal cells, PLO17 also inhibited IPSP conductances but did not affect EPSP amplitudes. In contrast to the lack of effect in rat pyramidal cells, trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate (100 nM) inhibited the late IPSP conductance without influencing the EPSP or the early IPSP conductance of guinea pig pyramidal cells. Dynorphin A (1-17) (0.01-10 microM) did not affect resting membrane properties or evoked synaptic conductances in either preparation. Mu receptor activationin the CA3 of rats and guinea pigs results in the inhibition of inhibitory synaptic input to pyramidal cells.(ABSTRACT TRUNCATED AT 250 WORDS)     

大鼠P_(3b)波实验研究

目的　探讨大鼠P3b波的特点及形成机制 ,为人类P3b波的研究提供动物模型及研究资料。方法　记录颅骨内、隔区、海马CA1区P3b波且同步记录相应脑区细胞群峰放电 ,并观察毁损隔区对海马CA1区P3b及细胞放电的影响。结果　在海马CA1区记录到的P3b波与其细胞放电呈正相关 ,隔区损毁后 ,海马CA1区P3b波及细胞群峰放电基本同步减弱直至消失。结论　海马CA1区细胞在靶声刺激后的群峰放电是P3b波产生的重要机制。隔区结构及功能的完整对海马CA1区P3b波形成有重要作用 ,进一步表明海马CA1区细胞对靶声刺激的群峰放电是P3b波产生的重要原因。     

Rational use of in vitro P-glycoprotein assays in drug discovery

The action of FK960 [N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate], a novel cognitive enhancer, on excitatory synaptic transmission in the hippocampus was investigated. Excitatory postsynaptic potentials (EPSPs) and currents (EPSCs) were recorded intracellularly from CA1 neurons in rat hippocampus using the "blind patch" variant of whole-cell recording. FK960 (100 nM) significantly increased the amplitude of the EPSP, which was unchanged when changeover was made to control artificial cerebrospinal fluid (aCSF). FK960 had no significant action on membrane potential, input resistance, or the early GABAergic inhibitory postsynaptic current. The decay phase of the excitatory postsynaptic current was not significantly altered by exposure to FK960, indicating that the properties of desensitization and/or deactivation were unchanged and suggesting that the action of FK960 was unlikely to be the result of changes in the properties of the postsynaptic (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptors. The quantal content of the EPSP (1/CV(2)) increased after exposure to FK960 but not to control aCSF. Methyllycaconitine or alpha-bungarotoxin blocked the modulatory action of FK960 on the EPSP, and the finding that these alpha 7-nicotinic acetylcholine receptor (alpha 7nAChR) antagonists were effective raises the possibility that FK960 up-regulates the contribution of acetylcholine to synaptic efficacy in the hippocampus. It is concluded that FK960 increases the quantal release of glutamate from Schaffer collateral-commissural nerve terminals in area CA1 of the hippocampus either by changing the ambient level of acetylcholine or by positively modulating the activity of alpha 7nAChRs located on glutamatergic nerve terminals.     

有无妄想精神分裂症患者事件相关位P300亚成分研究

目的研究有妄想与无妄想精神分裂症患者事件相关电位P300亚成分的异同。方法采用美国Nicolet Bravo脑电生理仪,检测50例精神分裂症患者及50例正常对照的P300亚成分,并运用阳性和阴性症状量表（Positive and Negative Syndrome Scale,PANSS）,对患者进行精4神症状的评定,按PANSS量表中阳性量表P1项得分≥3分者归入有妄想组,其余归入无妄想组。结果两组与正常对照比较,在四个记录区,P3a、P3b波幅下降,差异有统计学意义（P〈0．01）。两组比较,无妄想组,P3a波幅在C3、Pz区降低,差异有统计学意义（P〈0．05）,P3b波幅在四个记录区,均降低,差异有统计学意义（P〈0．05）。结论精神分裂症患者存在认知功能的损害,无妄想组精神分裂症患者认知功能损害程度重。