| 1 | Eur Arch Psychiatry Clin Neurosci 2011年10月261日：477-82 |
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| PMID | 21328015 |
| Title | 氟哌啶醇和氯氮平对能量剥夺的OLN-93少突胶质细胞的保护作用。 |
| Abstract | 磁共振成像和验尸研究精神分裂症provided evidence for compromised myelin integrity and reduced numbers of oligodendrocytes, which may worsen during the disease course. However, it is not clear whether these findings result from disease-inherent oligodendrocyte degeneration or side effects of antipsychotic treatment. Therefore, effects of haloperidol and clozapine on the viability and apoptosis of immature oligodendrocytes (OLN-93 cells, immunopositive for NG2,olig1，在本研究中，通过用碘化丙啶和caspase 3测定法进行了评估。鉴于脑力供应受损的迹象精神分裂症与基础条件（BC）相比，选择了血清和葡萄糖剥夺（SGD）模型。SGD导致坏死和凋亡细胞死亡增加。氟哌啶醇和氯氮平在该模型中具有部分保护性，并降低了碘化丙啶阳性细胞的百分比，而caspase 3活性没有改变。在BC下未观察到明显的药物作用。观察到的氟哌啶醇和氯氮平对能量剥夺的OLN-93少突胶质细胞的保护作用表明，先前报道的先前报道的少突胶质细胞密度降低精神分裂症are rather disease related than a side effect of medication. A new mechanism of antipsychotic action is suggested, which may help to establish new oligodendrocyte-directed therapies of精神分裂症。 |
| SCZ Keywords | 精神分裂症 |
| 2 | 生命科学。2013年10月93日：429-34 |
| PMID | 23973956 |
| Title | Antipsychotics promote the differentiation of oligodendrocyte progenitor cells by regulating oligodendrocyte lineage transcription factors 1 and 2. |
| Abstract | 少突胶质细胞/髓磷脂异常可能是在精神分裂症。The aim of this current study was to examine the possible effects of the antipsychotic drugs (APDs) haloperidol (HAL), olanzapine (OLA), and quetiapine (QUE) on the development of oligodendroglial lineage cells. CG4 cells, an oligodendrocyte progenitor cell line, were treated with various concentrations of HAL, OLA, or QUE for specific periods. The proliferation and differentiation of the CG4 cells were measured. The regulation of CG4 cell differentiation by oligodendrocyte lineage transcription factors 1 and 2 (olig1和Olig2）进行了检查。 本研究中使用的美国没有影响proliferation of CG4 cells. The APDs elevated the expression of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP), a specific marker of oligodendrocytes, and promoted the CG4 cells to differentiate into CNP positive oligodendrocytes. QUE and OLA increased the expression of botholig1和olig2，而HAL仅增加了olig2的表达。 我们的发现表明，少突胶质细胞的发展是HAL，OLA和QUE的目标，并提供了进一步的证据，证明了少突胶质细胞在病理生理学和治疗的重要作用精神分裂症。他们还表明，少突胶质细胞/髓磷脂相关基因的表达水平可能受到APD的深刻影响，应在未来的研究中考虑，旨在测量少突胶质细胞/髓磷脂相关基因表达式精神分裂症patients. |
| SCZ Keywords | 精神分裂症 |
| 3 | J Psychiatr Res 2013 8月47日：1069-79 |
| PMID | 23615187 |
| Title | 大抑郁症患者的前扣带回白质的核olig1表达增加：补偿少突胶质细胞损失的再生尝试？ |
| Abstract | Structural and functional oligodendrocyte deficits as well as impaired myelin integrity have been described in affective disorders and精神分裂症，并可能干扰与疾病相关的大脑区域之间的连通性。olig1, an oligodendroglial transcription factor, might be important in this context, but has not been systematically studied so far. Nissl- andolig1在骨前扣带回（PACC）/背外侧前额叶皮层（DLPFC）中定量 - 染色的少突胶质细胞，并在重大抑郁症患者（MDD，N. =�9），双极疾病（BD，N。8），，精神分裂症(SZ, n�=�13), and matched controls (n�=�16). Potential downstream effects of increasedolig1-expression were analyzed. Antidepressant drug effects onolig1- 在OLN-93少突胶质细胞培养物中进一步探索了表达。 两个白质区域的NISSL染色显示，MDD和BD中总的少突胶质密度降低了19-27％，但在SZ中却没有降低。相反，核olig1-immunoreactivity was elevated in MDD in the pACC-adjacent white matter (left: p�=�0.008; right: p�=�0.018); this effect tended to increase with antidepressant dosage (r�=�0.631, p�=�0.069). This reactive increase ofolig1通过丙咪嗪和阿米替林在少突胶质细胞培养物中的部分剂量依赖性作用证实。相应地，PACC染色的白质中的MBP表达往往会随着抗抑郁剂剂量而增加（r。= =�0.637，p = =�0.065）。其他经过测试的大脑区域没有依赖诊断的差异olig1-immunoreactivity. 自核olig1- 表达标志着少突胶质细胞前体细胞，其表达增加以及MDD患者PACC染色的白质的总少突胶质细胞密度（NISSL染色）降低，可能表明（预先促进药物的）重新生产尝试以补偿少突胶质细胞的再生尝试。 |
| SCZ Keywords | 精神分裂症 |
| 4 | 前细胞Neurosci 2016 -1 10：78 |
| PMID | 27065804 |
| Title | Oligodendrocyte and Interneuron Density in Hippocampal Subfields in Schizophrenia and Association of Oligodendrocyte Number with Cognitive Deficits. |
| Abstract | 在精神分裂症, previous stereological post-mortem investigations of anterior, posterior, and total hippocampal subfields showed no alterations in total neuron number but did show decreased oligodendrocyte numbers in CA4, an area that corresponds to the polymorph layer of the dentate gyrus (DG). However, these investigations identified oligodendrocytes only on the basis of morphological criteria in Nissl staining and did not assess alterations of interneurons with immunohistochemical markers. Moreover, the association of findings in the posterior hippocampus with cognitive deficits remains unknown. On the basis of the available clinical records, we compared patients with definite and possible cognitive dysfunction; nine patients had evidence in their records of either definite (n = 4) or possible (n = 5) cognitive dysfunction. Additionally, we assessed the density of two oligodendrocyte subpopulations immunostained by the oligodendrocyte transcription factorsolig1和Olig2和由白蛋白蛋白免疫标记的中间神经元。我们调查了同一后大脑的后海马后区精神分裂症患者（SZ; n = 10）和健康对照（n = 10）我们在先前发表的立体研究中检查了。我们的立体学研究发现，左侧（p = 0.014）和右（p = 0.050）CA4（p = 0.050）（p = 0.050）的明确认知缺陷的患者总/NISSL染色的少突胶质细胞数量减少了（p = 0.050）（p = 0.050）（p = 0.050）（p = 0.050）（p= 0.027），与具有认知缺陷的患者相比，海马前部的左（p = 0.050）和右（p = 0.014）下部（p = 0.014）。在本研究中，我们发现海马后部没有明确的认知缺陷的显着影响，而在整个海马SZ中，具有确定认知缺陷的整个海马SZ显示左侧的少突胶质细胞数量降低（p = 0.050）和右（p = 0.050）（p = 0.050））DG和左CA2/3（P = 0.050）。我们没有发现在olig1- 在后海马的任何子区域中，SZ和对照之间的Olig2-或白蛋白阳性细胞密度。根据我们的立体学研究的结果，我们假设在前和整个海马中的少突胶质细胞数量减少，可能会通过损害这种结构在该结构中的连通性而参与认知缺陷。精神分裂症。在海马后，我们无法复制先前报道的整个海马中间神经元的发现。 |
| SCZ Keywords | 精神分裂症 |