| 1 | 经验。神经。2001年11月172日：29-46 |
|---|---|
| PMID | 11681838 |
| Title | 人类裂解的N-CAM和精神分裂症的缔合的表征。 |
| 抽象的 | 神经细胞粘附分子（N-CAM）是与细胞迁移，突触可塑性和CNS发育有关的细胞识别分子。N-CAM的105至115 kDA同工型（裂解的N-CAM或CN-CAM）增加schizophrenia在海马，前额叶皮层和CSF中。我们纯化并部分表征了CN-CAM，这是一种假定的小型同工型，并确认前9个氨基酸与N-CAM的外显子1相同，而没有信号序列。通过基质辅助激光解吸电离在飞行时间质谱仪（MALDI-TOF）上分析胰蛋白酶消化的CN-CAM片段，产生的肽可以识别为从前548个预期N的氨基酸残基。-CAM氨基酸序列。免疫学鉴定，具有针对细胞质，分泌的，可变的替代外显子或GPIepitopes failed to indicate other known splice variants. Neuraminidase treatment of cN-CAM produced a minor alteration resulting in a faster migrating immunoreactive band, indicating partial glycosylation of cN-CAM. Membranous particles from cytosolic brain extract containing cN-CAM were obtained by ultracentrifugation; however, CSF contained few such particles. cN-CAM and synaptophysin were colocalized on these particles. Both cN-CAM and N-CAM 180 were present in synaptosomal preparations of human brain. Following incubation of synaptosomes or brain tissue without protease inhibitors, N-CAM 180 was degraded and cN-CAM was increased. A cN-CAM-like band was present in human fetal neuronal cultures, but not in fetal astrocyte cultures. Thus, cN-CAM represents a protease- and neuraminidase-susceptible fragment possibly derived by proteolytic cleavage of N-CAM 180. An enlargement in ventricular volume in a group of adult patients withschizophreniaover a 2-year interval was found to be correlated with CSF cN-CAM levels as measured at the time of the initial MRI scan (r = 0.53, P = 0.01). cN-CAM is associated with ventricular enlargement; thus, the release of N-CAM fragments may be part of the pathogenic mechanism ofschizophreniain vulnerable brain regions such as the hippocampus and prefrontal cortex. Alternatively, the increases in cN-CAM inschizophrenia可能反映了蛋白水解或细胞外基质稳定性的更一般异常。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 2 | Hum. Mutat. 2004 Dec 24: 534-5 |
| PMID | 15532024 |
| Title | 突变的勿动蛋白- 66 (RTN4R)基因在受体schizophrenia. |
| 抽象的 | schizophrenia（SCZD）或精神分裂性疾病是Digeorge/Velo-Cardio-Facio综合征（DGS/VCFS）患者的普遍特征，这是由于染色体22Q11.2染色体带来的疾病。我们评估了NOGO-66受体基因（RTN4R），该基因映射在DGS/VCFS关键区域中，作为潜在的候选者schizophreniasusceptibility. RTN4R encodes for a functional cell surface receptor, a glycosylphosphatidylinositol (GPI)-linked protein, with multiple leucine-rich repeats (LRR), which is implicated in axonal growth inhibition. One hundred and twenty unrelated Italianschizophrenicpatients were screened for mutations in the RTN4R gene using denaturing high performance liquid chromatography (DHPLC). Three mutant alleles were detected, including two missense changes (c.355C>T; R119W and c.587G>A; R196H), and one synonymous codon variant (c.54G>A; L18L). The twoschizophrenicpatients with the missense changes were strongly resistant to the neuroleptic treatment at any dosage. Both missense changes were absent in 300 control subjects. Molecular modeling revealed that both changes lead to putative structural alterations of the native protein. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 3 | Hum. Mutat. 2004 Dec 24: 534-5 |
| PMID | 15532024 |
| Title | 突变的勿动蛋白- 66 (RTN4R)基因在受体schizophrenia. |
| 抽象的 | schizophrenia（SCZD）或精神分裂性疾病是Digeorge/Velo-Cardio-Facio综合征（DGS/VCFS）患者的普遍特征，这是由于染色体22Q11.2染色体带来的疾病。我们评估了NOGO-66受体基因（RTN4R），该基因映射在DGS/VCFS关键区域中，作为潜在的候选者schizophreniasusceptibility. RTN4R encodes for a functional cell surface receptor, a glycosylphosphatidylinositol (GPI)-linked protein, with multiple leucine-rich repeats (LRR), which is implicated in axonal growth inhibition. One hundred and twenty unrelated Italianschizophrenicpatients were screened for mutations in the RTN4R gene using denaturing high performance liquid chromatography (DHPLC). Three mutant alleles were detected, including two missense changes (c.355C>T; R119W and c.587G>A; R196H), and one synonymous codon variant (c.54G>A; L18L). The twoschizophrenicpatients with the missense changes were strongly resistant to the neuroleptic treatment at any dosage. Both missense changes were absent in 300 control subjects. Molecular modeling revealed that both changes lead to putative structural alterations of the native protein. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 4 | Schizophr. Res. 2005 Mar 73: 229-33 |
| PMID | 15653265 |
| Title | Globus pallidus volume is related to symptom severity in neuroleptic naive patients with schizophrenia. |
| 抽象的 | 这项研究比较了神经蛋白酶的天真幼稚患者schizophreniaand healthy controls using structural MRI. The volume of the external segment of the GP (GPe) was positively correlated with the severity of global symptoms, as measured by the Scale for the Assessment of Negative Symptoms and Scale for the Assessment of Positive Symptoms (SANS/SAPS, Andreasen and Olsen, 1982). The volume for the GP, GPe, and internal segment (GPI) did not differ between groups. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 5 | J Neural Transm (Vienna) 2008 May 115: 761-71 |
| PMID | 18188498 |
| Title | 精神分裂症，躁郁症和抑郁症中细胞prion蛋白（PRP（C））的表达。 |
| 抽象的 | Cellular prion protein (PrP(c)) is a copper-binding, membrane-attachedGPI-anchored glycoprotein characterized by a high degree of amino acid sequence conservation among mammals. PrP(c) expression has been demonstrated in neurons, microglia, lymphocytes, and keratinocytes. Recently, the concept that PrP(c) may be involved in the defense against oxidative stress was advanced. In the present study, we used immunohistochemistry for PrP(c) to investigate 60 brains from the Stanley Neuropathology Consortium (15 controls, 15 patients withschizophrenia, 15 with bipolar disorder, and 15 with major depression). Rating scores as well as the numerical density of PrP(c)-positive and -negative neurons and glial cells were determined in the cingulate gyrus. All four groups showed a very high interindividual variation. PrP(c)-positive glial cells were significantly reduced in the white matter of patients withschizophrenia，躁郁症和严重抑郁症。使用评分量表，双极患者的白质也获得了类似的结果。从混杂的变量中，使用药物（即抗精神病药，抗抑郁药和情绪稳定剂）对神经元和神经胶质细胞的PRP（C）表达产生了显着影响。在所有检查组中，白质神经胶质细胞的PRP（C） - 免疫反应率显着降低。但是，结果并不表示发生在大脑中的氧化应激schizophrenicand bipolar patients. Since the effect of antipsychotic and antidepressant medication as well as of mood stabilizers on the expression of PrP(c) was significant, it needs further clarification in experimental models. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 6 | J Neural Transm (Vienna) 2008 May 115: 761-71 |
| PMID | 18188498 |
| Title | 精神分裂症，躁郁症和抑郁症中细胞prion蛋白（PRP（C））的表达。 |
| 抽象的 | Cellular prion protein (PrP(c)) is a copper-binding, membrane-attachedGPI-anchored glycoprotein characterized by a high degree of amino acid sequence conservation among mammals. PrP(c) expression has been demonstrated in neurons, microglia, lymphocytes, and keratinocytes. Recently, the concept that PrP(c) may be involved in the defense against oxidative stress was advanced. In the present study, we used immunohistochemistry for PrP(c) to investigate 60 brains from the Stanley Neuropathology Consortium (15 controls, 15 patients withschizophrenia, 15 with bipolar disorder, and 15 with major depression). Rating scores as well as the numerical density of PrP(c)-positive and -negative neurons and glial cells were determined in the cingulate gyrus. All four groups showed a very high interindividual variation. PrP(c)-positive glial cells were significantly reduced in the white matter of patients withschizophrenia，躁郁症和严重抑郁症。使用评分量表，双极患者的白质也获得了类似的结果。从混杂的变量中，使用药物（即抗精神病药，抗抑郁药和情绪稳定剂）对神经元和神经胶质细胞的PRP（C）表达产生了显着影响。在所有检查组中，白质神经胶质细胞的PRP（C） - 免疫反应率显着降低。但是，结果并不表示发生在大脑中的氧化应激schizophrenicand bipolar patients. Since the effect of antipsychotic and antidepressant medication as well as of mood stabilizers on the expression of PrP(c) was significant, it needs further clarification in experimental models. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 7 | 立体定向功能Neurosurg 2010 -1 88：105-8 |
| PMID | 20134209 |
| Title | Pallidotomy for severe tardive jaw-opening dystonia. |
| 抽象的 | 在Aschizophrenic严重的开口处患者肌张力障碍after chronic neuroleptic treatment. The dystonia led to sustained mandibular joint dislocation, and tracheotomy was performed after suffocation. The jaw-opening dystonia disappeared immediately following pallidotomy; the tracheotomy was closed, and he regained eating and speech ability. Analysis of the neuronal firing of the globus pallidus revealed low neuronal firing rates in the internal pallidum (GPI) and an irregular burst pattern of theGPIcells compared to those in Parkinson's disease. These results suggest that pallidotomy is a treatment option for tardive jaw-opening dystonia and that dystonia of this type is driven by abnormal neural activities in theGPI。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 8 | Behav. Brain Res. 2011 Jul 220: 281-7 |
| PMID | 21315767 |
| Title | Lesions of the entopeduncular nucleus in rats prevent apomorphine-induced deficient sensorimotor gating. |
| 抽象的 | 多巴胺诱导的多功能性和缺乏的感觉运动门控，以声音惊吓反应（ASR）的抑制（PPI）测量，用作神经精神疾病的动物模型，例如schizophrenia和图雷特综合症。我们在这里调查了大鼠肠核（EPN）的兴奋性病变（EPN）是否相当于人类的pallidus interus（GPI），将改善丙氨酸引起的PPI缺陷和多动症。此外，我们研究了EPN病变对认知，动机和运动技能的影响。在雄性Sprague Dawley大鼠中，双侧EPN病变是通过立体定向注射偶像苯甲酸酯（4？g磷酸盐缓冲盐水，PBS 4？g）或通过注射车辆PBS诱导的。一周后，对大鼠进行了学习和记忆（连续和延迟交替，T迷宫）的测试，以进行动机（渐进比率测试，断点为3分钟，Skinner Box）和运动技能（旋转杆）。此后，在皮下注射apomorphine（1.0mg/kg和媒介物）和运动活性（0.5mg/kg和车辆）后，测试了大鼠ASR（惊吓反应系统）的PPI（惊吓反应系统）。依替酸酯诱导的EPN病变不会影响学习和记忆，动机或运动技能。基础运动活性和PPI也没有受到影响，但是EPN病变改善了丙氨酸诱导的超量倒变和不足的PPI。这项工作表明，EPN在调节多巴胺激动剂引起的不足的感觉运动门控和超塑料的情况下的重要作用，而不会影响正常的行为功能。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 9 | Behav. Brain Res. 2012 Jun 232: 130-6 |
| PMID | 22425742 |
| Title | 大脑对大鼠肠核的深脑刺激可防止丙氨酸诱导的缺乏的感觉运动门控。 |
| 抽象的 | 药理学诱导的刻板印象和缺乏的感觉运动门控，以抑制的预抑制（PPI）为原始的惊吓反应（ASR），用作神经精神疾病常见的某些症状的内表型，例如schizophrenia和图雷特综合症（TS）等。我们在这里调查了大鼠肠核（EPN）的高频深脑刺激（DB）是否相当于人类的pallidus intrus（GPI), would improve PPI-deficits and stereotypies induced by the dopamine receptor agonist apomorphine. Electrodes were stereotactically implanted bilaterally in the EPN of 13 Sprague-Dawley rats. After one week of recovery the rats were stimulated with an amplitude 20% below their individual threshold for side effects (130 Hz, 80 ?s pulse width) or sham-stimulated for epochs of five days. At the end of each epoch the effect of ongoing stimulation or sham-stimulation on apomorphine-induced stereotypies (vehicle and 0.5 mg/kg) and deficient PPI (vehicle and 1.0 mg/kg) were tested. In nine rats, in which the full protocol could be applied and in which the electrode position was histologically confirmed in the target, EPN DBS did not affect baseline PPI but counteracted the apomorphine-induced PPI-deficit, while apomorphine-induced stereotypies were not affected by DBS. This work indicates an important role of the EPN in the modulation of apomorphine-induced deficient prepulse inhibition. This model may be useful to further investigate the pathophysiological of deficient sensorimotor gating and mechanisms of action of DBS in certain neuropsychiatric disorders. |
| SCZ Keywords | schizophrenia, schizophrenic |