抗精神病药物在少突胶质细胞发育中的毒性及促增殖和分化效应
|
摘要
精神分裂症是一类常见的、慢性的可导致精神残疾的疾病,主要以思维、情感、行为等多方面的障碍及精神活动的不协调为主要特点,其患病率大约为1%。可以给个人、家庭和社会带来巨大的痛苦和负担,因此对精神分裂症的合理治疗一直是一个重要课题。目前精神分裂症的治疗主要是应用抗精神病药物,包括典型抗精神病药物和非典型抗精神病药物。
少突胶质细胞功能障碍和死亡在精神分裂症等精神障碍及多发硬化等神经退行性病变的病理改变中具有重要作用。前期研究表明,上述疾病中白质和少突胶质细胞均存在一定的损伤和死亡。神经干细胞原代培养发现,抗精神病药物可明显增加少突胶质细胞的数量,并促进神经干细胞向成熟少突胶质细胞分化,但药物产生这种效果的具体机制尚不明确。此效应是否特异地作用于少突胶质细胞系,尚未阐明,本研究以大鼠少突胶质细胞系CG4细胞为研究对象,研究非典型抗精神病药物奎硫平和奥氮平以及典型抗精神病药物氟哌啶醇直接作用少突胶质前体细胞,探讨抗精神病药物对少突胶质细胞系的直接作用机制,进一步探索精神分裂症的发病机制,为更好地研发高效、副作用小的新型抗精神病药物提供理论依据和实验数据。
本研究结果表明,奎硫平、奥氮平和氟哌啶醇3种抗精神病药物对CG4细胞均无明显的促增殖作用,并在较高浓度和较长时间培养条件下对细胞具有毒性效应;这3种药物均具有促进CG4细胞向成熟少突胶质细胞分化的效应,非典型抗精神病药物奎硫平和奥氮平促少突胶质细胞分化效应可能由Olig1/Olig2(bHLH)转录因子介导,而典型抗精神病药物氟哌啶醇的促分化效应可能只通过Olig2转录因子介导。
In recent decades, with global socio-economic rapidly developing and pace of life expediting, people face with more pressure from family, life and work, then leading to increasing number of people suffering from insomnia, anxiety, mania, depression, schizophrenia, Parkinson's and senile dementia and other neurological and psychiatric disorders. These kinds of diseases are mostly chronic and persistent, once onset would cause a great burden to the family and society, which has attracted extensive attention from the whole society and has become great challenges in the 21st century.
At present, antipsychotic drugs (APDs) are primarily treatment of mental disorders such as schizophrenia. However, some patients are not sensitive to drug treatment or lack of compliance, which cause residual symptoms, recurrence and companied with some other diseases. Most patients with schizophrenia require long-term or even lifelong treatment and support. Schizophrenia is one of the major diseases that consume more medical resources because of its high morbidity and recurrence rates in China. Recent years, the consumption of APDs has a clear upward trend. Comparing and selecting economic, safe and effective treatment for schizophrenia and assessing the prognosis of schizophrenia, which is currently the world's concern. The study of new atypical APDs has great significance, which not only help to solve problems of the typical APDs, but also can be used as a probe exploring human learning, work capacity and cognitive function.
Recent studies found that oligodendrocyte dysfunction and death plays an important role in the pathological changes of schizophrenia. In the CNS, myelin is synthesized by oligodendrocytes. The myelin coating of axons is a prerequisite for rapid impulse conduction and maintenance of axonal function. Whereas oligodendrocyte and myelin have important function and oligodendrocytes have a high susceptibility to injuries of the CNS, understanding mechanism of oligodendrocytes apoptosis and injury and exploring proliferation of remyelination can be new therapeutic strategies.
In this study, the subject is a rat oligodendrocyte cell line, CG4 cells, investigating a direct role of a typical APD haloperidol (HAL) and atypical APDs quetiapine (QUE) and olanzapine (OLA) on oligodendrocyte precursor cells, which can better explore the pathogenesis of schizophrenia and provide a theoretical basis and experimental data of studying new APDs.
Methods: Using MTT、CCK-8 assay and BrdU assay to test the toxicity and proliferation effects of APDs on CG4 cells, and using optical microscope, immunofluorescence staining and Western Blot to detect differentiation effects of APDs on CG4 cells.
Treatment of toxicity and proliferation effects on CG4 cells: CG4 cells were seeded into 96-well plates coated with PDL to culture for 16 h. Changing fresh medium (growth medium, GM) and adding APDs. Drug concentrations were as follows: 0, 0.01, 0.1, 1, 10 and 100μM. Placing plates into an incubator (5% CO2, 37℃), and then respectively testing 24 h, 48 h and 72 h results.
Treatment of differentiation effects on CG4 cells: CG4 cells were seeded into 6-well plates or chambers coated with PDL to culture for 16 h. Changing the GM to differentiation medium (DM), and adding the different concentration of APDs. Drug concentrations were as follows: 0, 0.01, 0.05, 0.1, 0.5 and 1μM. Placing plates or chambers into an incubator (5% CO2, 37℃) and after culturing more 3 days, then using optical microscope, immunofluorescence cytochemistry (ICC) staining and Western Blot to detect differentiation effects of APDs on CG4 cells.
Results: (1) Selection and identification of CG4 cell: CG4 cells originated in newborn rat cerebral cortex in primary culture, and derived from multipotential O2-A progenitor cells. It is an immortalized cell line, which can be unlimited passage. In this study, the CG4 cell line is provided by Manitoba University Neuropsychiatric Institute.
①Morphology of CG4 cells under microscope: In the growth medium, the morphology of CG4 cells are similar with oligodendrocytes which have smaller cell type; in the differentiation medium, after 3 days treatment, the morphology were multipolar- shaped structure and similar with the immature and mature oligodendrocytes.
②ICC staining results: In the growth medium, PDGFRαprotein was expressed as a marker of oligodendrocyte precursor cells (OPCs) in CG4 cells; in differentiation medium, after 3 days treatment, CNPase and MBP protein were expressed as markers of mature oligodendrocytes in CG4 cells.
(2) Toxicity and proliferation effects of APDs on CG4 cells:
①Toxicity: Higher concentrations and longer time treatment is toxic for CG4 cells.
②Proliferation: there were no proliferation effects of APDs on CG4 cells after 24 h, 48 h and 72 h treatment.
③Differentiation: After 3 days APDs inducement, the bipolar CG4 cells decreased, but multipolar shape cells increased. The percentage of processes > 3 group was higher than processes≤3 group both in control and APDs groups.
ICC results: After 3 days APDs inducement, PDGFRαexpressed lower and CNPase expressed higher in QUE (0.1μM, 3 d), OLA (1μM, 3 d) and HAL (0.5μM, 3 d) groups.
Western blot results:β-actin as a inner parameter, in QUE (0.1μM, 3 d), OLA (1μM, 3 d) and HAL (0.5μM, 3 d) groups, CNPase expressed higher and the difference is remarkable. PDGFRαexpressed lower and the difference of OLA group is prominent. Suggesting these 3 APDs have differentiation effects on CG4 cells.
When QUE=0.1μM, OLA=1μM and HAL=0.5μM, compared to control group (QUE/OLA/HAL=0) Olig2 had higher expression. Olig1 of QUE and OLA groups expressed higher and Olig 1 of HLA group also expressed higher but this difference is not marked. The differentiation effects of APDs on CG4 cells may be mediated by Olig1/ Olig2 (bHLH) transcription factors.
Conclusions: (1) In GM, CG4 cells morphologically showed a smaller cell bodies and bipolar processes, and expressed PDGFRα, Olig1 and Olig2, which have oligodendrocyte precursor cells characteristic. After 3 days induced in DM, CG4 cells morphologically showed multipolar processes, and expressed CNPase, MBP, Olig1 and Olig2, which have mature oligodendrocytes characteristic.
(2) Longer time and higher concentration of QUE (72 h, 100μM), OLA (100μM) and HAL (72 h, 10 and 100μM) treatment is toxic to CG4 cells.
(3) The time-effect curve and dose-effect curve showed that there was no proliferation effect of APDs treatment on CG4 cells.
(4) QUE (0.1μM, 3 d) and OLA (1μM, 3 d) can promote CG4 cells differentiation, even this effect may be mediated by Olig1/ Olig2 (bHLH) transcription factors.
(5) HAL (0.5μM, 3 d) can promote CG4 cells differentiation, even this effect may be mediated by Olig2 transcription factor.
The results suggest that, CG4 cells can be used as oligodendrocyte precursor cells in the cell line model. APDs can promote CG4 cells differentiation and the effects may be mediated by bHLH transcription factors.
New ideas in this study: To test direct effects of APDs on oligodendrocyte cell line CG4 cells first time in this study. The results in this study provide a certain amount of data to support further explore the mechanism of two types of antipsychotics. The results may in-depth promote exploration the pathogenesis of schizophrenia, and provide theoretical basis and experimental data to better develop efficient new antipsychotic drugs.
少突胶质细胞功能障碍和死亡在精神分裂症等精神障碍及多发硬化等神经退行性病变的病理改变中具有重要作用。前期研究表明,上述疾病中白质和少突胶质细胞均存在一定的损伤和死亡。神经干细胞原代培养发现,抗精神病药物可明显增加少突胶质细胞的数量,并促进神经干细胞向成熟少突胶质细胞分化,但药物产生这种效果的具体机制尚不明确。此效应是否特异地作用于少突胶质细胞系,尚未阐明,本研究以大鼠少突胶质细胞系CG4细胞为研究对象,研究非典型抗精神病药物奎硫平和奥氮平以及典型抗精神病药物氟哌啶醇直接作用少突胶质前体细胞,探讨抗精神病药物对少突胶质细胞系的直接作用机制,进一步探索精神分裂症的发病机制,为更好地研发高效、副作用小的新型抗精神病药物提供理论依据和实验数据。
本研究结果表明,奎硫平、奥氮平和氟哌啶醇3种抗精神病药物对CG4细胞均无明显的促增殖作用,并在较高浓度和较长时间培养条件下对细胞具有毒性效应;这3种药物均具有促进CG4细胞向成熟少突胶质细胞分化的效应,非典型抗精神病药物奎硫平和奥氮平促少突胶质细胞分化效应可能由Olig1/Olig2(bHLH)转录因子介导,而典型抗精神病药物氟哌啶醇的促分化效应可能只通过Olig2转录因子介导。
In recent decades, with global socio-economic rapidly developing and pace of life expediting, people face with more pressure from family, life and work, then leading to increasing number of people suffering from insomnia, anxiety, mania, depression, schizophrenia, Parkinson's and senile dementia and other neurological and psychiatric disorders. These kinds of diseases are mostly chronic and persistent, once onset would cause a great burden to the family and society, which has attracted extensive attention from the whole society and has become great challenges in the 21st century.
At present, antipsychotic drugs (APDs) are primarily treatment of mental disorders such as schizophrenia. However, some patients are not sensitive to drug treatment or lack of compliance, which cause residual symptoms, recurrence and companied with some other diseases. Most patients with schizophrenia require long-term or even lifelong treatment and support. Schizophrenia is one of the major diseases that consume more medical resources because of its high morbidity and recurrence rates in China. Recent years, the consumption of APDs has a clear upward trend. Comparing and selecting economic, safe and effective treatment for schizophrenia and assessing the prognosis of schizophrenia, which is currently the world's concern. The study of new atypical APDs has great significance, which not only help to solve problems of the typical APDs, but also can be used as a probe exploring human learning, work capacity and cognitive function.
Recent studies found that oligodendrocyte dysfunction and death plays an important role in the pathological changes of schizophrenia. In the CNS, myelin is synthesized by oligodendrocytes. The myelin coating of axons is a prerequisite for rapid impulse conduction and maintenance of axonal function. Whereas oligodendrocyte and myelin have important function and oligodendrocytes have a high susceptibility to injuries of the CNS, understanding mechanism of oligodendrocytes apoptosis and injury and exploring proliferation of remyelination can be new therapeutic strategies.
In this study, the subject is a rat oligodendrocyte cell line, CG4 cells, investigating a direct role of a typical APD haloperidol (HAL) and atypical APDs quetiapine (QUE) and olanzapine (OLA) on oligodendrocyte precursor cells, which can better explore the pathogenesis of schizophrenia and provide a theoretical basis and experimental data of studying new APDs.
Methods: Using MTT、CCK-8 assay and BrdU assay to test the toxicity and proliferation effects of APDs on CG4 cells, and using optical microscope, immunofluorescence staining and Western Blot to detect differentiation effects of APDs on CG4 cells.
Treatment of toxicity and proliferation effects on CG4 cells: CG4 cells were seeded into 96-well plates coated with PDL to culture for 16 h. Changing fresh medium (growth medium, GM) and adding APDs. Drug concentrations were as follows: 0, 0.01, 0.1, 1, 10 and 100μM. Placing plates into an incubator (5% CO2, 37℃), and then respectively testing 24 h, 48 h and 72 h results.
Treatment of differentiation effects on CG4 cells: CG4 cells were seeded into 6-well plates or chambers coated with PDL to culture for 16 h. Changing the GM to differentiation medium (DM), and adding the different concentration of APDs. Drug concentrations were as follows: 0, 0.01, 0.05, 0.1, 0.5 and 1μM. Placing plates or chambers into an incubator (5% CO2, 37℃) and after culturing more 3 days, then using optical microscope, immunofluorescence cytochemistry (ICC) staining and Western Blot to detect differentiation effects of APDs on CG4 cells.
Results: (1) Selection and identification of CG4 cell: CG4 cells originated in newborn rat cerebral cortex in primary culture, and derived from multipotential O2-A progenitor cells. It is an immortalized cell line, which can be unlimited passage. In this study, the CG4 cell line is provided by Manitoba University Neuropsychiatric Institute.
①Morphology of CG4 cells under microscope: In the growth medium, the morphology of CG4 cells are similar with oligodendrocytes which have smaller cell type; in the differentiation medium, after 3 days treatment, the morphology were multipolar- shaped structure and similar with the immature and mature oligodendrocytes.
②ICC staining results: In the growth medium, PDGFRαprotein was expressed as a marker of oligodendrocyte precursor cells (OPCs) in CG4 cells; in differentiation medium, after 3 days treatment, CNPase and MBP protein were expressed as markers of mature oligodendrocytes in CG4 cells.
(2) Toxicity and proliferation effects of APDs on CG4 cells:
①Toxicity: Higher concentrations and longer time treatment is toxic for CG4 cells.
②Proliferation: there were no proliferation effects of APDs on CG4 cells after 24 h, 48 h and 72 h treatment.
③Differentiation: After 3 days APDs inducement, the bipolar CG4 cells decreased, but multipolar shape cells increased. The percentage of processes > 3 group was higher than processes≤3 group both in control and APDs groups.
ICC results: After 3 days APDs inducement, PDGFRαexpressed lower and CNPase expressed higher in QUE (0.1μM, 3 d), OLA (1μM, 3 d) and HAL (0.5μM, 3 d) groups.
Western blot results:β-actin as a inner parameter, in QUE (0.1μM, 3 d), OLA (1μM, 3 d) and HAL (0.5μM, 3 d) groups, CNPase expressed higher and the difference is remarkable. PDGFRαexpressed lower and the difference of OLA group is prominent. Suggesting these 3 APDs have differentiation effects on CG4 cells.
When QUE=0.1μM, OLA=1μM and HAL=0.5μM, compared to control group (QUE/OLA/HAL=0) Olig2 had higher expression. Olig1 of QUE and OLA groups expressed higher and Olig 1 of HLA group also expressed higher but this difference is not marked. The differentiation effects of APDs on CG4 cells may be mediated by Olig1/ Olig2 (bHLH) transcription factors.
Conclusions: (1) In GM, CG4 cells morphologically showed a smaller cell bodies and bipolar processes, and expressed PDGFRα, Olig1 and Olig2, which have oligodendrocyte precursor cells characteristic. After 3 days induced in DM, CG4 cells morphologically showed multipolar processes, and expressed CNPase, MBP, Olig1 and Olig2, which have mature oligodendrocytes characteristic.
(2) Longer time and higher concentration of QUE (72 h, 100μM), OLA (100μM) and HAL (72 h, 10 and 100μM) treatment is toxic to CG4 cells.
(3) The time-effect curve and dose-effect curve showed that there was no proliferation effect of APDs treatment on CG4 cells.
(4) QUE (0.1μM, 3 d) and OLA (1μM, 3 d) can promote CG4 cells differentiation, even this effect may be mediated by Olig1/ Olig2 (bHLH) transcription factors.
(5) HAL (0.5μM, 3 d) can promote CG4 cells differentiation, even this effect may be mediated by Olig2 transcription factor.
The results suggest that, CG4 cells can be used as oligodendrocyte precursor cells in the cell line model. APDs can promote CG4 cells differentiation and the effects may be mediated by bHLH transcription factors.
New ideas in this study: To test direct effects of APDs on oligodendrocyte cell line CG4 cells first time in this study. The results in this study provide a certain amount of data to support further explore the mechanism of two types of antipsychotics. The results may in-depth promote exploration the pathogenesis of schizophrenia, and provide theoretical basis and experimental data to better develop efficient new antipsychotic drugs.
引文
[1]杨文明,赵广峰,董婷,等.帕金森病患者的睡眠障碍研究进展[J].中国实验方剂学杂志, 2009, 15 (12): 109-111.
[2]柏宁,岳长红,孙福川.近年来中国抑郁症高发的社会因素分析[J].医学与哲学(人文社会医学版), 2007, 25 (3): 26-27.
[3]王刚,郑呐,谭玉燕,等.帕金森病疾病经济负担及相关因素的调查研究[J].中华神经科杂志, 2006, 39 (5): 336-337.
[4]江开达.精神病学[M].北京:人民卫生出版社, 2005.
[5] PALMER CS, BRUNNER E, RUIZ-FLORES LG, et al. A Cost-Effectiveness Clinical Decision Analysis Model for Treatment of Schizophrenia [J]. Archives of Medical Research, 2002, 33 (6): 572-580.
[6] BLIN O. A comparative review of new antipsychotics [J]. Can J Psychiatry, 1999, 44 (3): 235-244.
[7]江开达.抗精神病药物的安全性及耐受性[J].上海精神医学, 2009, 21 (3): 129-132.
[8]李静.抗精神病药物的合理应用[J].中国处方药, 2007, (62): 45-49.
[9]贾裕堂.抗精神病药物作用于精神分裂症患者使用评估[J].中外健康文摘, 2007, 4 (9): 78-81.
[10]王洪军.抗精神病药物的临床应用[J].内蒙古民族大学学报(自然科学版), 2008, 23 (5): 588-591.
[11]吴彦,施慎逊.抗精神病药物的评价与临床选择[J].上海医药, 2009, 30 (10): 444-447.
[12] FRIEDMAN JI, TEMPORINI H, DAVIS KL. Pharmacologic strategies for augmenting cognitive performance in schizophrenia [J]. Biological Psychiatry, 1999, 45 (1): 1-16.
[13] DAVIS JM, CHEN N, GLICK ID. A Meta-analysis of the Efficacy of Second Generation Antipsychotics [J]. Arch Gen Psychiatry, 2003, 60 (6): 553-564.
[14] WALKER E, KESTLER L, BOLLINI A, et al. Schizophrenia: Etiology and Course [J]. Annual Review of Psychology, 2004, 55 (1): 401-430.
[15] BOZIKAS VP, KOSMIDIS MH, KIOSSEOGLOU G, et al. Neuropsychological profile of cognitively impaired patients with schizophrenia [J]. Comprehensive Psychiatry, 2006, 47 (2): 136-143.
[16] CUESTA MJ, PERALTA V, ZARZUELA A. Effects of olanzapine and other antipsychotics on cognitive function in chronic schizophrenia: a longitudinal study [J]. Schizophrenia Research, 2001, 48 (1): 17-28.
[17] FIORAVANTI M, CARLONE O, VITALE B, et al. A Meta-Analysis of Cognitive Deficits in Adults with a Diagnosis of Schizophrenia [J]. Neuropsychology Review, 2005, 15 (2): 73-95.
[18] LEWIS DA, LIEBERMAN JA. Catching Up on Schizophrenia: Natural History and Neurobiology [J]. Neuron, 2000, 28 (2): 325-334.
[19] MIYAMOTO S, MAILMAN RB, LIEBERMAN JA, et al. Blunted brain metabolic response to ketamine in mice lacking D1A dopamine receptors [J]. Brain Research, 2001, 894 (2): 167-180.
[20] OKADA T, TOICHI M, SAKIHAMA M. Influences of an anticholinergic antiparkinsonian drug, parkinsonism, and psychotic symptoms on cardiac autonomic function in schizophrenia [J]. J Clin Psychopharmacol, 2003, 23 (5): 441-447.
[21] TAJIMA K, FERNáNDEZ H, LóPEZ-IBOR J, et al. Schizophrenia treatment: Critical review on the drugs and mechanisms of action of antipsychotics [J]. Actas Esp Psiquiatr, 2009, 37 (6): 330-342.
[22] DI LORENZO R, TONDELLI G, GENEDANI S. Effectiveness of clozapine and olanzapine: a comparison in severe, psychotically ill patients [J]. The International Journal of Neuropsychopharmacology, 2001, 4 (2): 135-137.
[23] LEUCHT S, KOMOSSA K, RUMMEL-KLUGE C, et al. A Meta-Analysis of Head-to- Head Comparisons of Second-Generation Antipsychotics in the Treatment of Schizophrenia [J]. Am J Psychiatry, 2009, 166 (2): 152-163.
[24] MOTLOVáL, SPANIEL F, H?SCHL C, et al. Are There Any Differences in the Efficacy among Second Generation Antipsychotics in the Treatment of Schizophrenia and Related Disorders? [J]. Annals of Clinical Psychiatry: The official Journal of the American Academy of Clinical Psychiatrists, 2007, 19 (2): 133 - 143.
[25] TAYLOR D, PATON C, KERWIN R. The Maudsley Prescribing Guidelines [M]. 7th edition, 2003.
[26] LALONDE P. Evaluating antipsychotic medications: predictors of clinical effectiveness. Report of an expert review panel on efficacy and effectiveness [J]. Can J Psychiatry, 2003, 48 (3 Suppl 1): 3S-12S.
[27] GOODNICK PJ, SANTANA O, RODRIGUEZ L. Antipsychotics: impact on prolactin levels [J]. Expert Opinion on Pharmacotherapy, 2002, 3 (10): 1381-1391.
[28]蔡飒,陈一岳.抗精神病药物治疗的进展[J].现代食品与药品杂志, 2004, 14 (1): 1-7.
[29] PURDON S. Cognitive improvement in schizophrenia with novel antipsychotic medications [J]. Schizophr Res, 1999, 35 (Suppl): S51-60.
[30] VAN KAMMEN D, MARDER S. Serotonin-dopamine antagonists(typical or second-generation antipsychotics), in Kaplan and Sadock's Comprehensive Textbook of Psychiatry,7th ed [D], 2005.
[31] TANDON R, MILNER K, JIBSON M. Antipsychotics from theory to practice: integrating clinical and basic data [J]. J Clin Psychiatry, 1999, 60 (Suppl 8): 21-28.
[32] REYNOLDS GP, KIRK SL. Metabolic side effects of antipsychotic drug treatment - pharmacological mechanisms [J]. Pharmacology & Therapeutics, 2010, 125 (1): 169-179.
[33] DE LEON J, GREENLEE B, BARBER J, et al. Practical guidelines for the use of new generation antipsychotic drugs (except clozapine) in adult individuals with intellectual disabilities [J]. Research in Developmental Disabilities, 2008, 30 (4): 613-669.
[34] SMITH M, HOPKINS D, PEVELER RC, et al. First- v. second-generation antipsychotics and risk for diabetes in schizophrenia: systematic review and meta-analysis [J]. The British Journal of Psychiatry, 2008, 192 (6): 406-411.
[35] EMSLEY R, RANIWALLA J, BAILEY P, et al. A comparison of the effects of quetiapine ('seroquel') and haloperidol in schizophrenic patients with a history of and a demonstrated, partial response to conventional antipsychotic treatment. PRIZE Study Group [J]. Int Clin Psychopharmacol, 2000, 15 (3): 121-131.
[36] CUTLER A, GOLDSTEIN J, TUMAS J. Dosing and switching strategies for quetiapine fumarate [J]. Clin Ther, 2002, 24 (2): 209-222.
[37] CHEER SM, WAGSTAFF AJ. Quetiapine: A Review of Its Use in the Management of Schizophrenia [J]. CNS Drugs, 2004, 18 (3): 173-199.
[38] MENDHEKAR DN, SHARMA JB, SRILAKSHMI P. Use of Aripiprazole During Late Pregnancy in a Woman with Psychotic Illness [J]. Ann Pharmacother, 2006, 40 (3): 575.
[39] YANG CH, TSAI SJ, HWANG JP. The efficacy and safety of quetiapine for treatment of geriatric psychosis [J]. J Psychopharmacol, 2005, 19 (6): 661-666.
[40] DEV V, RANIWALLA J. Quetiapine: A Review of Its Safety in the Management of Schizophrenia [J]. Drug Safety, 2000, 23 (4): 295-307.
[41]宣洁琨.多巴胺D-3受体基因多态性与抗精神病药物疗效相关性研究[D].上海:上海交通大学硕士论文, 2007.
[42] DAVIS KL, STEWART DG, FRIEDMAN JI, et al. White Matter Changes in Schizophrenia: Evidence for Myelin-Related Dysfunction [J]. Arch Gen Psychiatry, 2003, 60 (5): 443-456.
[43] FERN? J, RAEDER MB, VIK-MO AO, et al. Antipsychotic drugs activate SREBP-regulated expression of lipid biosynthetic genes in cultured human glioma cells: a novel mechanism of action? [J]. Pharmacogenomics Journal, 2005, 5 (5): 298-304.
[44] MILLER RH. Regulation of oligodendrocyte development in the vertebrate CNS [J]. Progress in Neurobiology, 2002, 67 (6): 451-467.
[45] NICOLAY DJ, DOUCETTE JR, NAZARALI AJ. Transcriptional control of oligodendrogenesis [J]. Glia, 2007, 55 (13): 1287-1299.
[46] WEGNER M. A Matter of Identity: Transcriptional Control in Oligodendrocytes [J]. Journal of Molecular Neuroscience, 2008, 35 (1): 3-12.
[47] AGRESTI C, MEOMARTINI ME, AMADIO S, et al. ATP regulates oligoden- drocyte progenitor migration, proliferation, and differentiation: involvement of metabotropic P2 receptors [J]. Brain Research Reviews, 2005, 48 (2): 157-165.
[48] ARMSTRONG R. Isolation and characterization of immature oligodendrocyte lineage cells [J]. Methods, 1998, 16 (3): 282-292.
[49] BENARROCH EE. Oligodendrocytes: Susceptibility to injury and involvement in neurologic disease [J]. Neurology, 2009, 72 (20): 1779-1785.
[50] MCTIGUE DM, TRIPATHI RB. The life, death, and replacement of oligoden- drocytes in the adult CNS [J]. Journal of Neurochemistry, 2008, 107 (1): 1-19.
[51] SANCHEZ I, HASSINGER L, SIHAG RK, et al. Local Control of Neuro- filament Accumulation during Radial Growth of Myelinating Axons in Vivo: Selective Role of Site-Specific Phosphorylation [J]. J Cell Biol, 2000, 151 (5): 1013-1024.
[52] DUPREE J, MASON J, MARCUS J, et al. Oligodendrocytes assist in the maintenance of sodium channel clusters independent of the myelin sheath [J].Neuron Glia Biol, 2004, 1 (3): 179–192.
[53] EDGAR JM, MCLAUGHLIN M, YOOL D, et al. Oligodendroglial modulation of fast axonal transport in a mouse model of hereditary spastic paraplegia [J]. J Cell Biol, 2004, 166 (1): 121-131.
[54] KASSMANN CM, NAVE KA. Oligodendroglial impact on axonal function and survival - a hypothesis [J]. Current Opinion in Neurology, 2008, 21 (3): 235-241.
[55] SORTWELL CE, DALEY BF, PITZER MR, et al. Oligodendrocyte-type 2 astrocyte-derived trophic factors increase survival of developing dopamine neurons through the inhibition of apoptotic cell death [J]. The Journal of Comparative Neurology, 2000, 426 (1): 143-153.
[56] TANIIKE M, MOHRI I, EGUCHI N, et al. Perineuronal Oligodendrocytes Protect against Neuronal Apoptosis through the Production of Lipocalin-Type Prostaglandin D Synthase in a Genetic Demyelinating Model [J]. J Neurosci, 2002, 22 (12): 4885-4896.
[57] WILKINS A, MAJED H, LAYFIELD R, et al. Oligodendrocytes Promote Neuronal Survival and Axonal Length by Distinct Intracellular Mechanisms: A Novel Role for Oligodendrocyte-Derived Glial Cell Line-Derived Neurotrophic Factor [J]. J Neurosci, 2003, 23 (12): 4967-4974.
[58] DAI X, QU P, DREYFUS CF. Neuronal signals regulate neurotrophin expression in oligodendrocytes of the basal forebrain [J]. Glia, 2001, 34 (3): 234-239.
[59] WILKINS A, CHANDRAN S, COMPSTON A. A role for oligodendrocyte derived IGF-1 in trophic support of cortical neurons [J]. Glia, 2001, 36 (1): 48-57.
[60] DOUGHERTY KD, DREYFUS CF, BLACK IB. Brain-Derived Neurotrophic Factor in Astrocytes, Oligodendrocytes, and Microglia/Macrophages after Spinal Cord Injury [J]. Neurobiology of Disease, 2000, 7 (6): 574-585.
[61] DU Y, DREYFUS CF. Oligodendrocytes as providers of growth factors [J]. Journal of Neuroscience Research, 2002, 68 (6): 647-654.
[62] MCKERRACHER L, WINTON MJ. Nogo on the Go [J]. Neuron, 2002, 36 (3): 345-348.
[63] LU QR, SUN T, ZHU Z, et al. Common Developmental Requirement for Olig Function Indicates a Motor Neuron/Oligodendrocyte Connection [J]. Cell, 2002,109 (1): 75-86.
[64] SUN T, ECHELARD Y, LU R, et al. Olig bHLH proteins interact with homeodomain proteins to regulate cell fate acquisition in progenitors of the ventral neural tube [J]. Current Biology, 2001, 11 (18): 1413-1420.
[65] LIGON KL, ALBERTA JA, KHO AT, et al. The oligodendroglial lineage marker OLIG2 is universally expressed in diffuse gliomas [J]. J Neuropathol Exp Neurol, 2004, 63 (5): 499-509.
[66] AGUIRRE A, GALLO V. Postnatal Neurogenesis and Gliogenesis in the Olfactory Bulb from NG2-Expressing Progenitors of the Subventricular Zone [J]. J Neurosci, 2004, 24 (46): 10530-10541.
[67] HACK MA, SUGIMORI M, LUNDBERG C, et al. Regionalization and fate specification in neurospheres: the role of Olig2 and Pax6 [J]. Molecular and Cellular Neuroscience, 2004, 25 (4): 664-678.
[68] LIGON KL, FANCY SP, FRANKLIN RJ, et al. Olig gene function in CNS development and disease [J]. Glia, 2006, 54 (1): 1-10.
[69] GEORGIEVA L, MOSKVINA V, PEIRCE T, et al. Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia [J]. Proc Natl Acad Sci U S A, 2006, 103 (33): 12469-12474.
[70] HAKAK Y, WALKER J, LI C, et al. Genome-wide expression analysis reveals dysregulation of myelination-related genes in chronic schizophrenia [J]. Proc Natl Acad Sci U S A, 2001, 98 (8): 4746-4751.
[71] IWAMOTO K, BUNDO M, YAMADA K, et al. DNA Methylation Status of SOX10 Correlates with Its Downregulation and Oligodendrocyte Dysfunction in Schizophrenia [J]. J Neurosci, 2005, 25 (22): 5376-5381.
[72] KATSEL P, DAVIS KL, HAROUTUNIAN V. Variations in myelin and oligodendrocyte- related gene expression across multiple brain regions in schizophrenia: A gene ontology study [J]. Schizophrenia Research, 2005, 79 (2-3): 157-173.
[73] TKACHEV D, MIMMACK ML, RYAN MM, et al. Oligodendrocyte dysfunction in schizophrenia and bipolar disorder [J]. The Lancet, 2003, 362 (9386): 798-805.
[74] ARNETT HA, FANCY SP, ALBERTA JA, et al. bHLH transcription factor Olig1 is required to repair demyelinated lesions in the CNS [J]. Science, 2004,306 (5704): 2111-2115.
[75] ROSS SE, GREENBERG ME, STILES CD. Basic Helix-Loop-Helix Factors in Cortical Development [J]. Neuron, 2003, 39 (1): 13-25.
[76] BURTON A. Olig1 needed for remyelination [J]. The Lancet Neurology, 2005, 4 (2): 80-80.
[77] MATUTE C, ALBERDI E, DOMERCQ M, et al. Excitotoxic damage to white matter [J]. Journal of Anatomy, 2007, 210 (6): 693-702.
[78] BUTT AM. Neurotransmitter-mediated calcium signalling in oligodendrocyte physiology and pathology [J]. Glia, 2006, 54 (7): 666-675.
[79] KHWAJA O, VOLPE JJ. Pathogenesis of cerebral white matter injury of prematurity [J]. Arch Dis Child Fetal Neonatal Ed, 2008, 93 (2): F153–F161.
[80] KáRADóTTIR R, ATTWELL D. Neurotransmitter receptors in the life and death of oligodendrocytes [J]. Neuroscience, 2007, 145 (4): 1426-1438.
[81] BAKIRI Y, BURZOMATO V, FRUGIER G, et al. Glutamatergic signaling in the brain's white matter [J]. Neuroscience, 2009, 158 (1): 266-274.
[82] BARNETT MH, SUTTON I. The pathology of multiple sclerosis: a paradigm shift [J]. Current Opinion in Neurology, 2006, 19 (3): 242-247.
[83] GREGOR KW, NADIA S, KURT AJ, et al. Multiple system atrophy: A primary oligodendrogliopathy [J]. Annals of Neurology, 2008, 64 (3): 239-246.
[84] GROSSMAN SD, ROSENBERG LJ, WRATHALL JR. Temporal-Spatial Pattern of Acute Neuronal and Glial Loss after Spinal Cord Contusion [J]. Experimental Neurology, 2001, 168 (2): 273-282.
[85] MCTIGUE DM, WEI P, STOKES BT. Proliferation of NG2-Positive Cells and Altered Oligodendrocyte Numbers in the Contused Rat Spinal Cord [J]. J Neurosci, 2001, 21 (10): 3392-3400.
[86] EMERY E, ALDANA P, BUNGE MB, et al. Apoptosis after traumatic human spinal cord injury [J]. Journal of Neurosurgery, 1998, 89 (6): 911-920.
[87] CHOW B, LI Y, WONG C. Radiation-induced apoptosis in the adult central nervous system is p53-dependent [J]. Cell Death Differ, 2000, 7 (8): 712-720.
[88] ROTH A, RAMíREZ G, ALARCóN R, et al. Oligodendrocytes damage in Alzheimer's disease: beta amyloid toxicity and inflammation [J]. Biol Res, 2005, 38 (4): 381-387.
[89] SJ?BECK M, HAGLUND M, ENGLUND E. Decreasing myelin density reflected increasing white matter pathology in Alzheimer's disease --neuropathological study [J]. International Journal of Geriatric Psychiatry, 2005, 20 (10): 919-926.
[90] BARTZOKIS G, LU PH, NUECHTERLEIN KH, et al. Differential effects of typical and atypical antipsychotics on brain myelination in schizophrenia [J]. Schizophrenia Research, 2007, 93 (1-3): 13-22.
[91] URANOVA NA, VOSTRIKOV VM, VIKHREVA OV, et al. The role of oligodendrocyte pathology in schizophrenia [J]. The International Journal of Neuropsychopharmacology, 2007, 10 (04): 537-545.
[92] ZHANG Y, XU H, XIAO L, et al. Quetiapine alleviates the cuprizone-induced white matter pathology in the brain of C57BL/6 mouse [J]. Schizophrenia Research, 2008, 102 (1-3, Supplement 2): 67-68.
[93] SIMS R, HOLLINGWORTH P, MOSKVINA V, et al. Evidence that variation in the oligodendrocyte lineage transcription factor 2 (OLIG2) gene is associated with psychosis in Alzheimer's disease [J]. Neuroscience Letters, 2009, 461 (1): 54-59.
[94] XIAO L, XU H, ZHANG Y, et al. Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes [J]. Mol Psychiatry, 2008, 13 (7): 697-708.
[95] LIBLAU R, FONTAINE B, BARON-VAN EVERCOOREN A, et al. Demyelinating diseases: from pathogenesis to repair strategies [J]. Trends in Neurosciences, 2001, 24 (3): 134-135.
[96] LUDWIN SK. The pathobiology of the oligodendrocyte [J]. J Neuropathol Exp Neurol, 1997, 56 (2): 111-124.
[97] CONNOR J, MENZIES S. Relationship of iron to oligodendrocytes and myelination [J]. Glia, 1996, 17 (2): 83-93.
[98] MCLAURIN JA, YONG VW. Oligodendrocytes and myelin [J]. Neurol Clin, 1995, 13 (1): 23-49.
[99] WOSIK K, ANTEL J, KUHLMANN T, et al. Oligodendrocyte injury in multiple sclerosis: a role for p53 [J]. Journal of Neurochemistry, 2003, 85 (3): 635-644.
[100] MOUZANNAR R, MIRIC SJ, WIGGINS RC, et al. Hydrogen peroxide induces rapid digestion of oligodendrocyte chromatin into high molecular weight fragments [J]. Neurochemistry International, 2001, 38 (1): 9-15.
[101] UBERTI D, YAVIN E, GIL S, et al. Hydrogen peroxide induces nuclearneuropathological study [J]. International Journal of Geriatric Psychiatry, 2005, 20 (10): 919-926.
[90] BARTZOKIS G, LU PH, NUECHTERLEIN KH, et al. Differential effects of typical and atypical antipsychotics on brain myelination in schizophrenia [J]. Schizophrenia Research, 2007, 93 (1-3): 13-22.
[91] URANOVA NA, VOSTRIKOV VM, VIKHREVA OV, et al. The role of oligodendrocyte pathology in schizophrenia [J]. The International Journal of Neuropsychopharmacology, 2007, 10 (04): 537-545.
[92] ZHANG Y, XU H, XIAO L, et al. Quetiapine alleviates the cuprizone-induced white matter pathology in the brain of C57BL/6 mouse [J]. Schizophrenia Research, 2008, 102 (1-3, Supplement 2): 67-68.
[93] SIMS R, HOLLINGWORTH P, MOSKVINA V, et al. Evidence that variation in the oligodendrocyte lineage transcription factor 2 (OLIG2) gene is associated with psychosis in Alzheimer's disease [J]. Neuroscience Letters, 2009, 461 (1): 54-59.
[94] XIAO L, XU H, ZHANG Y, et al. Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes [J]. Mol Psychiatry, 2008, 13 (7): 697-708.
[95] LIBLAU R, FONTAINE B, BARON-VAN EVERCOOREN A, et al. Demyelinating diseases: from pathogenesis to repair strategies [J]. Trends in Neurosciences, 2001, 24 (3): 134-135.
[96] LUDWIN SK. The pathobiology of the oligodendrocyte [J]. J Neuropathol Exp Neurol, 1997, 56 (2): 111-124.
[97] CONNOR J, MENZIES S. Relationship of iron to oligodendrocytes and myelination [J]. Glia, 1996, 17 (2): 83-93.
[98] MCLAURIN JA, YONG VW. Oligodendrocytes and myelin [J]. Neurol Clin, 1995, 13 (1): 23-49.
[99] WOSIK K, ANTEL J, KUHLMANN T, et al. Oligodendrocyte injury in multiple sclerosis: a role for p53 [J]. Journal of Neurochemistry, 2003, 85 (3): 635-644.
[100] MOUZANNAR R, MIRIC SJ, WIGGINS RC, et al. Hydrogen peroxide induces rapid digestion of oligodendrocyte chromatin into high molecular weight fragments [J]. Neurochemistry International, 2001, 38 (1): 9-15.
[101] UBERTI D, YAVIN E, GIL S, et al. Hydrogen peroxide induces nuclear(12): 1978-1994.
[114] POSSE DE CHAVES EI. Sphingolipids in apoptosis, survival and regeneration in the nervous system [J]. Biochimica et Biophysica Acta (BBA) - Biomembranes, 2006, 1758 (12): 1995-2015.
[115] SCHENCK M, CARPINTEIRO A, GRASSM H, et al. Ceramide: Physiological and pathophysiological aspects [J]. Archives of Biochemistry and Biophysics, 2007, 462 (2): 171-175.
[116] AKTAS O, PROZOROVSKI T, ZIPP F. Death Ligands and Autoimmune Demyelination [J]. Neuroscientist, 2006, 12 (4): 305-316.
[117] BROGI A, STRAZZA M, MELLI M, et al. Induction of intracellular ceramide by interleukin-1 beta in oligodendrocytes [J]. Journal of Cellular Biochemistry, 1997, 66 (4): 532-541.
[118] TESTAI FD, LANDEK MA, Dawson G. Regulation of sphingomyelinases in cells of the oligodendrocyte lineage [J]. Journal of Neuroscience Research, 2004, 75 (1): 66-74.
[119] CASACCIA-BONNEFIL P, AIBEL L, CHAO MV. Central glial and neuronal populations display differential sensitivity to ceramide-dependent cell death [J]. J Neurosci Res, 1996, 43 (3): 382-389.
[120] CASACCIA-BONNEFIL P, CARTER B, DOBROWSKY R, et al. Death of oligodendrocytes mediated by the interaction of nerve growth factor with its receptor p75 [J]. Nature, 1996, 383 (6602): 716-719.
[121] CASACCIA-BONNEFIL P. Cell death in the oligodendrocyte lineage: A molecular perspective of life/death decisions in development and disease [J]. Glia, 2000, 29 (2): 124-135.
[122] LAROCCA J, FAROOQ M, NORTON W. Induction of oligodendrocyte apoptosis by C2-ceramide [J]. Neurochem Res, 1997, 22 (4): 529-534.
[123] LEE JT, XU J, LEE JM, et al. Amyloid-{beta} peptide induces oligodendrocyte death by activating the neutral sphingomyelinase-ceramide pathway [J]. J Cell Biol, 2004, 164 (1): 123-131.
[124] JANA A, PAHAN K. Oxidative Stress Kills Human Primary Oligodendrocytes Via Neutral Sphingomyelinase: Implications for Multiple Sclerosis [J]. Journal of Neuroimmune Pharmacology, 2007, 2 (2): 184-193.
[125] SINGH I, PAHAN K, KHAN M, et al. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatorycytokine-mediated apoptosis in demyelinating diseases [J]. J Biol Chem, 1998, 273 (32): 20354-20362.
[126] MATTSON M. Excitotoxic and excitoprotective mechanisms [J]. NeuroMolecular Medicine, 2003, 3 (2): 65-94.
[127] PARK E, VELUMIAN AA, FEHLINGS MG. The Role of Excitotoxicity in Secondary Mechanisms of Spinal Cord Injury: A Review with an Emphasis on the Implications for White Matter Degeneration [J]. Journal of Neurotrauma, 2004, 21 (6): 754-774.
[128] LI S, MEALING G, MORLEY P, et al. Novel injury mechanism in anoxia and trauma of spinal cord white matter: glutamate release via reverse Na+-dependent glutamate transport [J]. J Neurosci, 1999, 19 (14): RC16.
[129] FERN R, MOLLER T. Rapid Ischemic Cell Death in Immature Oligodendrocytes: A Fatal Glutamate Release Feedback Loop [J]. J Neurosci, 2000, 20 (1): 34-42.
[130] BARGER SW, GOODWIN ME, PORTER MM, et al. Glutamate release from activated microglia requires the oxidative burst and lipid peroxidation [J]. Journal of Neurochemistry, 2007, 101 (5): 1205-1213.
[131] DOMERCQ M, SANCHEZ-GOMEZ MV, SHERWIN C, et al. System xc- and Glutamate Transporter Inhibition Mediates Microglial Toxicity to Oligodendrocytes [J]. J Immunol, 2007, 178 (10): 6549-6556.
[132] MATUTE C, ALBERDI E, IBARRETXE G, et al. Excitotoxicity in glial cells [J]. European Journal of Pharmacology, 2002, 447 (2-3): 239-246.
[133] DENG W, YUE Q, ROSENBERG PA, et al. Oligodendrocyte excitotoxicity determined by local glutamate accumulation and mitochondrial function [J]. Journal of Neurochemistry, 2006, 98 (1): 213-222.
[134] ALBERDI E, SANCHEZ-GOMEZ MV, TORRE I, et al. Activation of Kainate Receptors Sensitizes Oligodendrocytes to Complement Attack [J]. J Neurosci, 2006, 26 (12): 3220-3228.
[135] LI S, STYS PK. Mechanisms of Ionotropic Glutamate Receptor-Mediated Excitotoxicity in Isolated Spinal Cord White Matter [J]. J Neurosci, 2000, 20 (3): 1190-1198.
[136] SáNCHEZ-GóMEZ MV, MATUTE C. AMPA and Kainate Receptors Each Mediate Excitotoxicity in Oligodendroglial Cultures [J]. Neurobiology of Disease, 1999, 6 (6): 475-485.
[137] TANAKA H, GROOMS SY, BENNETT MVL, et al. The AMPAR subunit GluR2: still front and center-stage [J]. Brain Research, 2000, 886 (1-2): 190-207.
[138] HISAHARA S, SHOJI SI, OKANO H. ICE/CED-3 Family Executes Oligo- dendrocyte Apoptosis by Tumor Necrosis Factor [J]. Journal of Neurochemistry, 1997, 69 (1): 10-20.
[139] CURATOLO L, VALSASINA B, CACCIA C, et al. Recombinant human IL-2 is cytotoxic to oligodendrocytes after in vitro self aggregation [J]. Cytokine, 1997, 9 (10): 734-739.
[140] JUREWICZ A, MATYSIAK M, TYBOR K, et al. Tumour necrosis factor-induced death of adult human oligodendrocytes is mediated by apoptosis inducing factor [J]. Brain, 2005, 128 (11): 2675-2688.
[141] MERRILL, SCOLDING. Mechanisms of damage to myelin and oligodendro- cytes and their relevance to disease [J]. Neuropathology & Applied Neurobiology, 1999, 25 (6): 435-458.
[142] BELKA C, BUDACH W, KORTMANN RD, et al. Radiation induced CNS toxicity--molecular and cellular mechanisms [J]. Br J Cancer, 2001, 85 (9): 1233-1239.
[143] KURITA H, KAWAHARA N, ASAI A, et al. Radiation-induced apoptosis of oligodendrocytes in the adult rat brain [J]. Neurol Res, 2001, 23 (8): 869-874.
[144] HAQ E, GIRI S, SINGH I, et al. Molecular mechanism of psychosine induced cell death in human oligodendrocyte cell line [J]. Journal of Neurochemistry, 2003, 86 (6): 1428-1440.
[145] KHAN M, HAQ E, GIRI S, et al. Peroxisomal participation in psychosine mediated toxicity: Implications for Krabbe's disease [J]. Journal of Neuroscience Research, 2005, 80 (6): 845-854.
[146] GIRI S, KHAN M, RATTAN R, et al. Krabbe disease: psychosine-mediated activation of phospholipase A2 in oligodendrocyte cell death [J]. J Lipid Res, 2006, 47 (7): 1478-1492.
[147] JUNG M, SOMMER I, SCHACHNER M, et al. Monoclonal Antibody O10 Defines a Conformationally Sensitive Cell-Surface Epitope of Proteolipid Protein (PLP): Evidence that PLP Misfolding Underlies Dysmyelination in Mutant Mice [J]. J Neurosci, 1996, 16 (24): 7920-7929.
[148] PAK K, CHAN S, MATTSON M. Presenilin-1 mutation sensitizes oligoden-drocytes to glutamate and amyloid toxicities, and exacerbates white matter damage and memory impairment in mice [J]. NeuroMolecular Medicine, 2003, 3 (1): 53-64.
[149] QUINLAN RA, BRENNER M, GOLDMAN JE, et al. GFAP and its role in Alexander disease [J]. Experimental Cell Research, 2007, 313 (10): 2077-2087.
[150] MIGNOT C, BOESPFLUG-TANGUY O, GELOT A, et al. Alexander disease: putative mechanisms of an astrocytic encephalopathy [J]. Cellular and Molecular Life Sciences, 2004, 61 (3): 369-385.
[151] MOSER H, DUBEY P, FATEMI A. Progress in X-linked adrenoleuko- dystrophy [J]. Curr Opin Neurol, 2004, 17 (3): 263-269.
[152] Feigenbaum V, Gélot A, Casanova P, et al. Apoptosis in the Central Nervous System of Cerebral Adrenoleukodystrophy Patients [J]. Neurobiology of Disease, 2000, 7 (6): 600-612.
[153] ITO M, BLUMBERG B, MOCK D, et al. Potential environmental and host participants in the early white matter lesion of adreno-leukodystrophy: morphologic evidence for CD8 cytotoxic T cells, cytolysis of oligodendrocytes, and CD1-mediated lipid antigen presentation [J]. J Neuropathol Exp Neurol, 2001, 60 (10): 1004-1019.
[154] ARNETT H, MASON J, MARINO M, et al. TNF alpha promotes proliferation of oligodendrocyte progenitors and remyelination [J]. Nat Neurosci, 2001, 4 (11): 1116-1122.
[155] MASON JL, SUZUKI K, CHAPLIN DD, et al. Interleukin-1{beta} Promotes Repair of the CNS [J]. J Neurosci, 2001, 21 (18): 7046-7052.
[156] LOUIS J, MAGAL E, MUIR D, et al. CG-4, a new bipotential glial cell line from rat brain, is capable of differentiating in vitro into either mature oligodendrocytes or type-2 astrocytes [J]. J Neurosci Res, 1992, 31 (1): 193-204.
[157] NGUYEN D, H?PFNER M, ZOBEL F, et al. Rat oligodendroglial cell lines express a functional receptor for the chemokine CCL3 (macrophage inflammatory protein-1alpha) [J]. Neuroscience Letters, 2003, 351 (2): 71-74.
[158] YAO S, PANDEY P, LJUNGGREN-ROSE A, et al. LPS mediated injury to oligodendrocytes is mediated by the activation of nNOS: relevance to human demyelinating disease [J]. Nitric Oxide, 2010, 22 (3): 197-204.
[159] BARNETT M, PRINEAS J. Relapsing and remitting multiple sclerosis:pathology of the newly forming lesion [J]. Ann Neurol, 2004, 55 (4): 458-468.
[160] COMPSTON A, COLES A. Multiple sclerosis [J]. The Lancet, 2008, 372 (9648): 1502-1517.
[161] BRüCK W. The pathology of multiple sclerosis is the result of focal inflammatory demyelination with axonal damage [J]. Journal of Neurology, 2005, 252 (0): v3-v9.
[162] FREEDMAN R. Schizophrenia [J]. N Engl J Med, 2003, 349 (18): 1738-1749.
[163] SAWA A, SNYDER S. Schizophrenia: diverse approaches to a complex disease [J]. Science, 2003, 296 (5568): 692-695.
[164] MARTINS-DE-SOUZA D. Proteome and transcriptome analysis suggests oligodendrocyte dysfunction in schizophrenia [J]. J Psychiatr Res, 2010, 44 (3): 149-156.
[165] PRICE G, CERCIGNANI M, CHU EM, et al. Brain pathology in first episode psychosis: Magnetization transfer imaging provides additional information to MRI measurements of volume loss [J]. NeuroImage, 2010, 49 (1): 185-192.
[166] KUBICKI M, PARK H, WESTIN CF, et al. DTI and MTR abnormalities in schizophrenia: Analysis of white matter integrity [J]. NeuroImage, 2005, 26 (4): 1109-1118.
[167] URANOVA N, ORLOVSKAYA D, VIKHREVA O, et al. Electron microscopy of oligodendroglia in severe mental illness [J]. Brain Research Bulletin, 2001, 55 (5): 597-610.
[168] SCHMITT A, WILCZEK K, BLENNOW K, et al. Altered thalamic membrane phospholipids in schizophrenia: a postmortem study [J]. Biological Psychiatry, 2004, 56 (1): 41-45.
[169] LIU X, QIN W, HE G, et al. A family-based association study of the MOG gene with schizophrenia in the Chinese population [J]. Schizophrenia Research, 2005, 73 (2-3): 275-280.
[170] HOF PR, HAROUTUNIAN V, FRIEDRICH VL, et al. Loss and altered spatial distribution of oligodendrocytes in the superior frontal gyrus in schizophrenia [J]. Biological Psychiatry, 2003, 53 (12): 1075-1085.
[171] KAROUTZOU G, EMRICH HM, DIETRICH DE. The myelin-pathogenesis puzzle in schizophrenia: a literature review [J]. Mol Psychiatry, 2008, 13 (3): 245-260.
[172] MALBERG JE, EISCH AJ, NESTLER EJ, et al. Chronic AntidepressantTreatment Increases Neurogenesis in Adult Rat Hippocampus [J]. J Neurosci, 2000, 20 (24): 9104-9110.
[173] DUMAN RS, MALBERG J, NAKAGAWA S, et al. Neuronal plasticity and survival in mood disorders [J]. Biological Psychiatry, 2000, 48 (8): 732-739.
[174] SANTARELLI L, SAXE M, GROSS C, et al. Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants [J]. Science, 2003, 301 (5634): 805-809.
[175] MALBERG JE, DUMAN RS. Cell Proliferation in Adult Hippocampus is Decreased by Inescapable Stress: Reversal by Fluoxetine Treatment [J]. Neuropsychopharmacology, 2003, 28 (9): 1562-1571.
[176] WAKADE CG, MAHADIK SP, WALLER JL, et al. Atypical neuroleptics stimulate neurogenesis in adult rat brain [J]. Journal of Neuroscience Research, 2002, 69 (1): 72-79.
[177] HALIM ND, WEICKERT CS, MCCLINTOCK BW, et al. Effects of Chronic Haloperidol and Clozapine Treatment on Neurogenesis in the Adult Rat Hippocampus [J]. Neuropsychopharmacology, 2004, 29 (6): 1063-1069.
[178] SCHMITT A, WEBER S, JATZKO A, et al. Hippocampal volume and cell proliferation after acute and chronic clozapine or haloperidol treatment [J]. Journal of Neural Transmission, 2004, 111 (1): 91-100.
[179] WANG H-D, DUNNAVANT FD, JARMAN T, et al. Effects of Antipsychotic Drugs on Neurogenesis in the Forebrain of the Adult Rat [J]. Neuropsychopharmacology, 2004, 29 (7): 1230-1238.
[180] KIPPIN TE, KAPUR S, VAN DER KOOY D. Dopamine Specifically Inhibits Forebrain Neural Stem Cell Proliferation, Suggesting a Novel Effect of Antipsychotic Drugs [J]. J Neurosci, 2005, 25 (24): 5815-5823.
[181] VOSTRIKOV VM, URANOVA NA, ORLOVSKAYA DD. Deficit of perineuronal oligodendrocytes in the prefrontal cortex in schizophrenia and mood disorders [J]. Schizophrenia Research, 2007, 94 (1-3): 273-280.
[182] HAROUTUNIAN V, KATSEL P, DRACHEVA S, et al. Variations in oligodendrocyte- related gene expression across multiple cortical regions: implications for the pathophysiology of schizophrenia [J]. The International Journal of Neuropsychopharmacology, 2007, 10 (04): 565-573.
[183] MIMMACK M, RYAN M, BABA H, et al. Gene expression analysis in schizophrenia: reproducible up-regulation of several members of theapolipoprotein L family located in a high-susceptibility locus for schizophrenia on chromosome 22 [J]. Proc Natl Acad Sci U S A, 2002, 99 (7): 4680-4685.
[184] SANFILIPO M, LAFARGUE T, ARENA L, et al. Fine Volumetric Analysis of the Cerebral Ventricular System in Schizophrenia: Further Evidence for Multifocal Mild to Moderate Enlargement [J]. Schizophr Bull, 2000, 26 (1): 201-216.
[185] SIGMUNDSSON T, SUCKLING J, MAIER M, et al. Structural Abnormalities in Frontal, Temporal, and Limbic Regions and Interconnecting White Matter Tracts in Schizophrenic Patients With Prominent Negative Symptoms [J]. Am J Psychiatry, 2001, 158 (2): 234-243.
[186] BAGARY MS, SYMMS MR, BARKER GJ, et al. Gray and White Matter Brain Abnormalities in First-Episode Schizophrenia Inferred From Magneti- zation Transfer Imaging [J]. Arch Gen Psychiatry, 2003, 60 (8): 779-788.
[187] MATSUSHIMA GK, MORELL P. The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system. [J]. Brain Pathol, 2001, 1 (11): 107-116.
[188] KOMOLY S. Experimental demyelination caused by primary oligoden- drocyte dystrophy. Regional distribution of the lesions in the nervous system of mice [J]. Ideggyogy Sz, 2005, 58 (1-2): 40-43.
[189] HUILLARD E, ROWITCH DH. Olig2 function in adult neural stem and progenitor cells [J]. International Journal of Developmental Neuroscience, 2008, 26 (8): 872-872.
[190] HUANG K, TANG W, TANG R, et al. Positive association between OLIG2 and schizophrenia in the Chinese Han population [J]. Human Genetics, 2008, 122 (6): 659-660.
[191] LI H, LU Y, SMITH H, et al. Olig1 and Sox10 interact synergistically to drive myelin basic protein transcription in oligodendrocytes [J]. The Journal of Neuroscience, 2007 27 (52): 14375-14382.
[192] ZHOU Q, ANDERSON DJ. The bHLH Transcription Factors OLIG2 and OLIG1 Couple Neuronal and Glial Subtype Specification [J]. Cell, 2002, 109 (1): 61-73.
[193] HALL AK, MILLER RH. Emerging roles for bone morphogenetic proteins in central nervous system glial biology [J]. Journal of Neuroscience Research, 2004, 76 (1): 1-8.
[194] AGIUS E, SOUKKARIEH C, DANESIN C, et al. Converse control of oligodendrocyte and astrocyte lineage development by Sonic hedgehog in the chick spinal cord [J]. Developmental Biology, 2004, 270 (2): 308-321.
[195] GOMES WA, MEHLER MF, KESSLER JA. Transgenic overexpression of BMP4 increases astroglial and decreases oligodendroglial lineage commitment [J]. Developmental Biology, 2003, 255 (1): 164-177.
[196] CHENG X, WANG Y, HE Q, et al. Bone Morphogenetic Protein Signaling and Olig1/2 Interact to Regulate the Differentiation and Maturation of Adult Oligodendrocyte Precursor Cells [J]. Stem Cells, 2007, 25 (12): 3204-3214.
[197] ONO K, TAKEBAYASHI H, IKEDA K, et al. Regional- and temporal dependent changes in the differentiation of Olig2 progenitors in the forebrain, and the impact on astrocyte development in the dorsal pallium [J]. Developmental Biology, 2008, 320 (2): 456-468.
[198] KOUKO TATSUMI, TAKEBAYASHI H, MANABE T, et al. Genetic fate mapping of Olig2 progenitors in the injured adult cerebral cortex reveals preferential differentiation into astrocytes [J]. Journal of Neuroscience Research, 2008, 86 (16): 3494-3502.
[2]柏宁,岳长红,孙福川.近年来中国抑郁症高发的社会因素分析[J].医学与哲学(人文社会医学版), 2007, 25 (3): 26-27.
[3]王刚,郑呐,谭玉燕,等.帕金森病疾病经济负担及相关因素的调查研究[J].中华神经科杂志, 2006, 39 (5): 336-337.
[4]江开达.精神病学[M].北京:人民卫生出版社, 2005.
[5] PALMER CS, BRUNNER E, RUIZ-FLORES LG, et al. A Cost-Effectiveness Clinical Decision Analysis Model for Treatment of Schizophrenia [J]. Archives of Medical Research, 2002, 33 (6): 572-580.
[6] BLIN O. A comparative review of new antipsychotics [J]. Can J Psychiatry, 1999, 44 (3): 235-244.
[7]江开达.抗精神病药物的安全性及耐受性[J].上海精神医学, 2009, 21 (3): 129-132.
[8]李静.抗精神病药物的合理应用[J].中国处方药, 2007, (62): 45-49.
[9]贾裕堂.抗精神病药物作用于精神分裂症患者使用评估[J].中外健康文摘, 2007, 4 (9): 78-81.
[10]王洪军.抗精神病药物的临床应用[J].内蒙古民族大学学报(自然科学版), 2008, 23 (5): 588-591.
[11]吴彦,施慎逊.抗精神病药物的评价与临床选择[J].上海医药, 2009, 30 (10): 444-447.
[12] FRIEDMAN JI, TEMPORINI H, DAVIS KL. Pharmacologic strategies for augmenting cognitive performance in schizophrenia [J]. Biological Psychiatry, 1999, 45 (1): 1-16.
[13] DAVIS JM, CHEN N, GLICK ID. A Meta-analysis of the Efficacy of Second Generation Antipsychotics [J]. Arch Gen Psychiatry, 2003, 60 (6): 553-564.
[14] WALKER E, KESTLER L, BOLLINI A, et al. Schizophrenia: Etiology and Course [J]. Annual Review of Psychology, 2004, 55 (1): 401-430.
[15] BOZIKAS VP, KOSMIDIS MH, KIOSSEOGLOU G, et al. Neuropsychological profile of cognitively impaired patients with schizophrenia [J]. Comprehensive Psychiatry, 2006, 47 (2): 136-143.
[16] CUESTA MJ, PERALTA V, ZARZUELA A. Effects of olanzapine and other antipsychotics on cognitive function in chronic schizophrenia: a longitudinal study [J]. Schizophrenia Research, 2001, 48 (1): 17-28.
[17] FIORAVANTI M, CARLONE O, VITALE B, et al. A Meta-Analysis of Cognitive Deficits in Adults with a Diagnosis of Schizophrenia [J]. Neuropsychology Review, 2005, 15 (2): 73-95.
[18] LEWIS DA, LIEBERMAN JA. Catching Up on Schizophrenia: Natural History and Neurobiology [J]. Neuron, 2000, 28 (2): 325-334.
[19] MIYAMOTO S, MAILMAN RB, LIEBERMAN JA, et al. Blunted brain metabolic response to ketamine in mice lacking D1A dopamine receptors [J]. Brain Research, 2001, 894 (2): 167-180.
[20] OKADA T, TOICHI M, SAKIHAMA M. Influences of an anticholinergic antiparkinsonian drug, parkinsonism, and psychotic symptoms on cardiac autonomic function in schizophrenia [J]. J Clin Psychopharmacol, 2003, 23 (5): 441-447.
[21] TAJIMA K, FERNáNDEZ H, LóPEZ-IBOR J, et al. Schizophrenia treatment: Critical review on the drugs and mechanisms of action of antipsychotics [J]. Actas Esp Psiquiatr, 2009, 37 (6): 330-342.
[22] DI LORENZO R, TONDELLI G, GENEDANI S. Effectiveness of clozapine and olanzapine: a comparison in severe, psychotically ill patients [J]. The International Journal of Neuropsychopharmacology, 2001, 4 (2): 135-137.
[23] LEUCHT S, KOMOSSA K, RUMMEL-KLUGE C, et al. A Meta-Analysis of Head-to- Head Comparisons of Second-Generation Antipsychotics in the Treatment of Schizophrenia [J]. Am J Psychiatry, 2009, 166 (2): 152-163.
[24] MOTLOVáL, SPANIEL F, H?SCHL C, et al. Are There Any Differences in the Efficacy among Second Generation Antipsychotics in the Treatment of Schizophrenia and Related Disorders? [J]. Annals of Clinical Psychiatry: The official Journal of the American Academy of Clinical Psychiatrists, 2007, 19 (2): 133 - 143.
[25] TAYLOR D, PATON C, KERWIN R. The Maudsley Prescribing Guidelines [M]. 7th edition, 2003.
[26] LALONDE P. Evaluating antipsychotic medications: predictors of clinical effectiveness. Report of an expert review panel on efficacy and effectiveness [J]. Can J Psychiatry, 2003, 48 (3 Suppl 1): 3S-12S.
[27] GOODNICK PJ, SANTANA O, RODRIGUEZ L. Antipsychotics: impact on prolactin levels [J]. Expert Opinion on Pharmacotherapy, 2002, 3 (10): 1381-1391.
[28]蔡飒,陈一岳.抗精神病药物治疗的进展[J].现代食品与药品杂志, 2004, 14 (1): 1-7.
[29] PURDON S. Cognitive improvement in schizophrenia with novel antipsychotic medications [J]. Schizophr Res, 1999, 35 (Suppl): S51-60.
[30] VAN KAMMEN D, MARDER S. Serotonin-dopamine antagonists(typical or second-generation antipsychotics), in Kaplan and Sadock's Comprehensive Textbook of Psychiatry,7th ed [D], 2005.
[31] TANDON R, MILNER K, JIBSON M. Antipsychotics from theory to practice: integrating clinical and basic data [J]. J Clin Psychiatry, 1999, 60 (Suppl 8): 21-28.
[32] REYNOLDS GP, KIRK SL. Metabolic side effects of antipsychotic drug treatment - pharmacological mechanisms [J]. Pharmacology & Therapeutics, 2010, 125 (1): 169-179.
[33] DE LEON J, GREENLEE B, BARBER J, et al. Practical guidelines for the use of new generation antipsychotic drugs (except clozapine) in adult individuals with intellectual disabilities [J]. Research in Developmental Disabilities, 2008, 30 (4): 613-669.
[34] SMITH M, HOPKINS D, PEVELER RC, et al. First- v. second-generation antipsychotics and risk for diabetes in schizophrenia: systematic review and meta-analysis [J]. The British Journal of Psychiatry, 2008, 192 (6): 406-411.
[35] EMSLEY R, RANIWALLA J, BAILEY P, et al. A comparison of the effects of quetiapine ('seroquel') and haloperidol in schizophrenic patients with a history of and a demonstrated, partial response to conventional antipsychotic treatment. PRIZE Study Group [J]. Int Clin Psychopharmacol, 2000, 15 (3): 121-131.
[36] CUTLER A, GOLDSTEIN J, TUMAS J. Dosing and switching strategies for quetiapine fumarate [J]. Clin Ther, 2002, 24 (2): 209-222.
[37] CHEER SM, WAGSTAFF AJ. Quetiapine: A Review of Its Use in the Management of Schizophrenia [J]. CNS Drugs, 2004, 18 (3): 173-199.
[38] MENDHEKAR DN, SHARMA JB, SRILAKSHMI P. Use of Aripiprazole During Late Pregnancy in a Woman with Psychotic Illness [J]. Ann Pharmacother, 2006, 40 (3): 575.
[39] YANG CH, TSAI SJ, HWANG JP. The efficacy and safety of quetiapine for treatment of geriatric psychosis [J]. J Psychopharmacol, 2005, 19 (6): 661-666.
[40] DEV V, RANIWALLA J. Quetiapine: A Review of Its Safety in the Management of Schizophrenia [J]. Drug Safety, 2000, 23 (4): 295-307.
[41]宣洁琨.多巴胺D-3受体基因多态性与抗精神病药物疗效相关性研究[D].上海:上海交通大学硕士论文, 2007.
[42] DAVIS KL, STEWART DG, FRIEDMAN JI, et al. White Matter Changes in Schizophrenia: Evidence for Myelin-Related Dysfunction [J]. Arch Gen Psychiatry, 2003, 60 (5): 443-456.
[43] FERN? J, RAEDER MB, VIK-MO AO, et al. Antipsychotic drugs activate SREBP-regulated expression of lipid biosynthetic genes in cultured human glioma cells: a novel mechanism of action? [J]. Pharmacogenomics Journal, 2005, 5 (5): 298-304.
[44] MILLER RH. Regulation of oligodendrocyte development in the vertebrate CNS [J]. Progress in Neurobiology, 2002, 67 (6): 451-467.
[45] NICOLAY DJ, DOUCETTE JR, NAZARALI AJ. Transcriptional control of oligodendrogenesis [J]. Glia, 2007, 55 (13): 1287-1299.
[46] WEGNER M. A Matter of Identity: Transcriptional Control in Oligodendrocytes [J]. Journal of Molecular Neuroscience, 2008, 35 (1): 3-12.
[47] AGRESTI C, MEOMARTINI ME, AMADIO S, et al. ATP regulates oligoden- drocyte progenitor migration, proliferation, and differentiation: involvement of metabotropic P2 receptors [J]. Brain Research Reviews, 2005, 48 (2): 157-165.
[48] ARMSTRONG R. Isolation and characterization of immature oligodendrocyte lineage cells [J]. Methods, 1998, 16 (3): 282-292.
[49] BENARROCH EE. Oligodendrocytes: Susceptibility to injury and involvement in neurologic disease [J]. Neurology, 2009, 72 (20): 1779-1785.
[50] MCTIGUE DM, TRIPATHI RB. The life, death, and replacement of oligoden- drocytes in the adult CNS [J]. Journal of Neurochemistry, 2008, 107 (1): 1-19.
[51] SANCHEZ I, HASSINGER L, SIHAG RK, et al. Local Control of Neuro- filament Accumulation during Radial Growth of Myelinating Axons in Vivo: Selective Role of Site-Specific Phosphorylation [J]. J Cell Biol, 2000, 151 (5): 1013-1024.
[52] DUPREE J, MASON J, MARCUS J, et al. Oligodendrocytes assist in the maintenance of sodium channel clusters independent of the myelin sheath [J].Neuron Glia Biol, 2004, 1 (3): 179–192.
[53] EDGAR JM, MCLAUGHLIN M, YOOL D, et al. Oligodendroglial modulation of fast axonal transport in a mouse model of hereditary spastic paraplegia [J]. J Cell Biol, 2004, 166 (1): 121-131.
[54] KASSMANN CM, NAVE KA. Oligodendroglial impact on axonal function and survival - a hypothesis [J]. Current Opinion in Neurology, 2008, 21 (3): 235-241.
[55] SORTWELL CE, DALEY BF, PITZER MR, et al. Oligodendrocyte-type 2 astrocyte-derived trophic factors increase survival of developing dopamine neurons through the inhibition of apoptotic cell death [J]. The Journal of Comparative Neurology, 2000, 426 (1): 143-153.
[56] TANIIKE M, MOHRI I, EGUCHI N, et al. Perineuronal Oligodendrocytes Protect against Neuronal Apoptosis through the Production of Lipocalin-Type Prostaglandin D Synthase in a Genetic Demyelinating Model [J]. J Neurosci, 2002, 22 (12): 4885-4896.
[57] WILKINS A, MAJED H, LAYFIELD R, et al. Oligodendrocytes Promote Neuronal Survival and Axonal Length by Distinct Intracellular Mechanisms: A Novel Role for Oligodendrocyte-Derived Glial Cell Line-Derived Neurotrophic Factor [J]. J Neurosci, 2003, 23 (12): 4967-4974.
[58] DAI X, QU P, DREYFUS CF. Neuronal signals regulate neurotrophin expression in oligodendrocytes of the basal forebrain [J]. Glia, 2001, 34 (3): 234-239.
[59] WILKINS A, CHANDRAN S, COMPSTON A. A role for oligodendrocyte derived IGF-1 in trophic support of cortical neurons [J]. Glia, 2001, 36 (1): 48-57.
[60] DOUGHERTY KD, DREYFUS CF, BLACK IB. Brain-Derived Neurotrophic Factor in Astrocytes, Oligodendrocytes, and Microglia/Macrophages after Spinal Cord Injury [J]. Neurobiology of Disease, 2000, 7 (6): 574-585.
[61] DU Y, DREYFUS CF. Oligodendrocytes as providers of growth factors [J]. Journal of Neuroscience Research, 2002, 68 (6): 647-654.
[62] MCKERRACHER L, WINTON MJ. Nogo on the Go [J]. Neuron, 2002, 36 (3): 345-348.
[63] LU QR, SUN T, ZHU Z, et al. Common Developmental Requirement for Olig Function Indicates a Motor Neuron/Oligodendrocyte Connection [J]. Cell, 2002,109 (1): 75-86.
[64] SUN T, ECHELARD Y, LU R, et al. Olig bHLH proteins interact with homeodomain proteins to regulate cell fate acquisition in progenitors of the ventral neural tube [J]. Current Biology, 2001, 11 (18): 1413-1420.
[65] LIGON KL, ALBERTA JA, KHO AT, et al. The oligodendroglial lineage marker OLIG2 is universally expressed in diffuse gliomas [J]. J Neuropathol Exp Neurol, 2004, 63 (5): 499-509.
[66] AGUIRRE A, GALLO V. Postnatal Neurogenesis and Gliogenesis in the Olfactory Bulb from NG2-Expressing Progenitors of the Subventricular Zone [J]. J Neurosci, 2004, 24 (46): 10530-10541.
[67] HACK MA, SUGIMORI M, LUNDBERG C, et al. Regionalization and fate specification in neurospheres: the role of Olig2 and Pax6 [J]. Molecular and Cellular Neuroscience, 2004, 25 (4): 664-678.
[68] LIGON KL, FANCY SP, FRANKLIN RJ, et al. Olig gene function in CNS development and disease [J]. Glia, 2006, 54 (1): 1-10.
[69] GEORGIEVA L, MOSKVINA V, PEIRCE T, et al. Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia [J]. Proc Natl Acad Sci U S A, 2006, 103 (33): 12469-12474.
[70] HAKAK Y, WALKER J, LI C, et al. Genome-wide expression analysis reveals dysregulation of myelination-related genes in chronic schizophrenia [J]. Proc Natl Acad Sci U S A, 2001, 98 (8): 4746-4751.
[71] IWAMOTO K, BUNDO M, YAMADA K, et al. DNA Methylation Status of SOX10 Correlates with Its Downregulation and Oligodendrocyte Dysfunction in Schizophrenia [J]. J Neurosci, 2005, 25 (22): 5376-5381.
[72] KATSEL P, DAVIS KL, HAROUTUNIAN V. Variations in myelin and oligodendrocyte- related gene expression across multiple brain regions in schizophrenia: A gene ontology study [J]. Schizophrenia Research, 2005, 79 (2-3): 157-173.
[73] TKACHEV D, MIMMACK ML, RYAN MM, et al. Oligodendrocyte dysfunction in schizophrenia and bipolar disorder [J]. The Lancet, 2003, 362 (9386): 798-805.
[74] ARNETT HA, FANCY SP, ALBERTA JA, et al. bHLH transcription factor Olig1 is required to repair demyelinated lesions in the CNS [J]. Science, 2004,306 (5704): 2111-2115.
[75] ROSS SE, GREENBERG ME, STILES CD. Basic Helix-Loop-Helix Factors in Cortical Development [J]. Neuron, 2003, 39 (1): 13-25.
[76] BURTON A. Olig1 needed for remyelination [J]. The Lancet Neurology, 2005, 4 (2): 80-80.
[77] MATUTE C, ALBERDI E, DOMERCQ M, et al. Excitotoxic damage to white matter [J]. Journal of Anatomy, 2007, 210 (6): 693-702.
[78] BUTT AM. Neurotransmitter-mediated calcium signalling in oligodendrocyte physiology and pathology [J]. Glia, 2006, 54 (7): 666-675.
[79] KHWAJA O, VOLPE JJ. Pathogenesis of cerebral white matter injury of prematurity [J]. Arch Dis Child Fetal Neonatal Ed, 2008, 93 (2): F153–F161.
[80] KáRADóTTIR R, ATTWELL D. Neurotransmitter receptors in the life and death of oligodendrocytes [J]. Neuroscience, 2007, 145 (4): 1426-1438.
[81] BAKIRI Y, BURZOMATO V, FRUGIER G, et al. Glutamatergic signaling in the brain's white matter [J]. Neuroscience, 2009, 158 (1): 266-274.
[82] BARNETT MH, SUTTON I. The pathology of multiple sclerosis: a paradigm shift [J]. Current Opinion in Neurology, 2006, 19 (3): 242-247.
[83] GREGOR KW, NADIA S, KURT AJ, et al. Multiple system atrophy: A primary oligodendrogliopathy [J]. Annals of Neurology, 2008, 64 (3): 239-246.
[84] GROSSMAN SD, ROSENBERG LJ, WRATHALL JR. Temporal-Spatial Pattern of Acute Neuronal and Glial Loss after Spinal Cord Contusion [J]. Experimental Neurology, 2001, 168 (2): 273-282.
[85] MCTIGUE DM, WEI P, STOKES BT. Proliferation of NG2-Positive Cells and Altered Oligodendrocyte Numbers in the Contused Rat Spinal Cord [J]. J Neurosci, 2001, 21 (10): 3392-3400.
[86] EMERY E, ALDANA P, BUNGE MB, et al. Apoptosis after traumatic human spinal cord injury [J]. Journal of Neurosurgery, 1998, 89 (6): 911-920.
[87] CHOW B, LI Y, WONG C. Radiation-induced apoptosis in the adult central nervous system is p53-dependent [J]. Cell Death Differ, 2000, 7 (8): 712-720.
[88] ROTH A, RAMíREZ G, ALARCóN R, et al. Oligodendrocytes damage in Alzheimer's disease: beta amyloid toxicity and inflammation [J]. Biol Res, 2005, 38 (4): 381-387.
[89] SJ?BECK M, HAGLUND M, ENGLUND E. Decreasing myelin density reflected increasing white matter pathology in Alzheimer's disease --neuropathological study [J]. International Journal of Geriatric Psychiatry, 2005, 20 (10): 919-926.
[90] BARTZOKIS G, LU PH, NUECHTERLEIN KH, et al. Differential effects of typical and atypical antipsychotics on brain myelination in schizophrenia [J]. Schizophrenia Research, 2007, 93 (1-3): 13-22.
[91] URANOVA NA, VOSTRIKOV VM, VIKHREVA OV, et al. The role of oligodendrocyte pathology in schizophrenia [J]. The International Journal of Neuropsychopharmacology, 2007, 10 (04): 537-545.
[92] ZHANG Y, XU H, XIAO L, et al. Quetiapine alleviates the cuprizone-induced white matter pathology in the brain of C57BL/6 mouse [J]. Schizophrenia Research, 2008, 102 (1-3, Supplement 2): 67-68.
[93] SIMS R, HOLLINGWORTH P, MOSKVINA V, et al. Evidence that variation in the oligodendrocyte lineage transcription factor 2 (OLIG2) gene is associated with psychosis in Alzheimer's disease [J]. Neuroscience Letters, 2009, 461 (1): 54-59.
[94] XIAO L, XU H, ZHANG Y, et al. Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes [J]. Mol Psychiatry, 2008, 13 (7): 697-708.
[95] LIBLAU R, FONTAINE B, BARON-VAN EVERCOOREN A, et al. Demyelinating diseases: from pathogenesis to repair strategies [J]. Trends in Neurosciences, 2001, 24 (3): 134-135.
[96] LUDWIN SK. The pathobiology of the oligodendrocyte [J]. J Neuropathol Exp Neurol, 1997, 56 (2): 111-124.
[97] CONNOR J, MENZIES S. Relationship of iron to oligodendrocytes and myelination [J]. Glia, 1996, 17 (2): 83-93.
[98] MCLAURIN JA, YONG VW. Oligodendrocytes and myelin [J]. Neurol Clin, 1995, 13 (1): 23-49.
[99] WOSIK K, ANTEL J, KUHLMANN T, et al. Oligodendrocyte injury in multiple sclerosis: a role for p53 [J]. Journal of Neurochemistry, 2003, 85 (3): 635-644.
[100] MOUZANNAR R, MIRIC SJ, WIGGINS RC, et al. Hydrogen peroxide induces rapid digestion of oligodendrocyte chromatin into high molecular weight fragments [J]. Neurochemistry International, 2001, 38 (1): 9-15.
[101] UBERTI D, YAVIN E, GIL S, et al. Hydrogen peroxide induces nuclearneuropathological study [J]. International Journal of Geriatric Psychiatry, 2005, 20 (10): 919-926.
[90] BARTZOKIS G, LU PH, NUECHTERLEIN KH, et al. Differential effects of typical and atypical antipsychotics on brain myelination in schizophrenia [J]. Schizophrenia Research, 2007, 93 (1-3): 13-22.
[91] URANOVA NA, VOSTRIKOV VM, VIKHREVA OV, et al. The role of oligodendrocyte pathology in schizophrenia [J]. The International Journal of Neuropsychopharmacology, 2007, 10 (04): 537-545.
[92] ZHANG Y, XU H, XIAO L, et al. Quetiapine alleviates the cuprizone-induced white matter pathology in the brain of C57BL/6 mouse [J]. Schizophrenia Research, 2008, 102 (1-3, Supplement 2): 67-68.
[93] SIMS R, HOLLINGWORTH P, MOSKVINA V, et al. Evidence that variation in the oligodendrocyte lineage transcription factor 2 (OLIG2) gene is associated with psychosis in Alzheimer's disease [J]. Neuroscience Letters, 2009, 461 (1): 54-59.
[94] XIAO L, XU H, ZHANG Y, et al. Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes [J]. Mol Psychiatry, 2008, 13 (7): 697-708.
[95] LIBLAU R, FONTAINE B, BARON-VAN EVERCOOREN A, et al. Demyelinating diseases: from pathogenesis to repair strategies [J]. Trends in Neurosciences, 2001, 24 (3): 134-135.
[96] LUDWIN SK. The pathobiology of the oligodendrocyte [J]. J Neuropathol Exp Neurol, 1997, 56 (2): 111-124.
[97] CONNOR J, MENZIES S. Relationship of iron to oligodendrocytes and myelination [J]. Glia, 1996, 17 (2): 83-93.
[98] MCLAURIN JA, YONG VW. Oligodendrocytes and myelin [J]. Neurol Clin, 1995, 13 (1): 23-49.
[99] WOSIK K, ANTEL J, KUHLMANN T, et al. Oligodendrocyte injury in multiple sclerosis: a role for p53 [J]. Journal of Neurochemistry, 2003, 85 (3): 635-644.
[100] MOUZANNAR R, MIRIC SJ, WIGGINS RC, et al. Hydrogen peroxide induces rapid digestion of oligodendrocyte chromatin into high molecular weight fragments [J]. Neurochemistry International, 2001, 38 (1): 9-15.
[101] UBERTI D, YAVIN E, GIL S, et al. Hydrogen peroxide induces nuclear(12): 1978-1994.
[114] POSSE DE CHAVES EI. Sphingolipids in apoptosis, survival and regeneration in the nervous system [J]. Biochimica et Biophysica Acta (BBA) - Biomembranes, 2006, 1758 (12): 1995-2015.
[115] SCHENCK M, CARPINTEIRO A, GRASSM H, et al. Ceramide: Physiological and pathophysiological aspects [J]. Archives of Biochemistry and Biophysics, 2007, 462 (2): 171-175.
[116] AKTAS O, PROZOROVSKI T, ZIPP F. Death Ligands and Autoimmune Demyelination [J]. Neuroscientist, 2006, 12 (4): 305-316.
[117] BROGI A, STRAZZA M, MELLI M, et al. Induction of intracellular ceramide by interleukin-1 beta in oligodendrocytes [J]. Journal of Cellular Biochemistry, 1997, 66 (4): 532-541.
[118] TESTAI FD, LANDEK MA, Dawson G. Regulation of sphingomyelinases in cells of the oligodendrocyte lineage [J]. Journal of Neuroscience Research, 2004, 75 (1): 66-74.
[119] CASACCIA-BONNEFIL P, AIBEL L, CHAO MV. Central glial and neuronal populations display differential sensitivity to ceramide-dependent cell death [J]. J Neurosci Res, 1996, 43 (3): 382-389.
[120] CASACCIA-BONNEFIL P, CARTER B, DOBROWSKY R, et al. Death of oligodendrocytes mediated by the interaction of nerve growth factor with its receptor p75 [J]. Nature, 1996, 383 (6602): 716-719.
[121] CASACCIA-BONNEFIL P. Cell death in the oligodendrocyte lineage: A molecular perspective of life/death decisions in development and disease [J]. Glia, 2000, 29 (2): 124-135.
[122] LAROCCA J, FAROOQ M, NORTON W. Induction of oligodendrocyte apoptosis by C2-ceramide [J]. Neurochem Res, 1997, 22 (4): 529-534.
[123] LEE JT, XU J, LEE JM, et al. Amyloid-{beta} peptide induces oligodendrocyte death by activating the neutral sphingomyelinase-ceramide pathway [J]. J Cell Biol, 2004, 164 (1): 123-131.
[124] JANA A, PAHAN K. Oxidative Stress Kills Human Primary Oligodendrocytes Via Neutral Sphingomyelinase: Implications for Multiple Sclerosis [J]. Journal of Neuroimmune Pharmacology, 2007, 2 (2): 184-193.
[125] SINGH I, PAHAN K, KHAN M, et al. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatorycytokine-mediated apoptosis in demyelinating diseases [J]. J Biol Chem, 1998, 273 (32): 20354-20362.
[126] MATTSON M. Excitotoxic and excitoprotective mechanisms [J]. NeuroMolecular Medicine, 2003, 3 (2): 65-94.
[127] PARK E, VELUMIAN AA, FEHLINGS MG. The Role of Excitotoxicity in Secondary Mechanisms of Spinal Cord Injury: A Review with an Emphasis on the Implications for White Matter Degeneration [J]. Journal of Neurotrauma, 2004, 21 (6): 754-774.
[128] LI S, MEALING G, MORLEY P, et al. Novel injury mechanism in anoxia and trauma of spinal cord white matter: glutamate release via reverse Na+-dependent glutamate transport [J]. J Neurosci, 1999, 19 (14): RC16.
[129] FERN R, MOLLER T. Rapid Ischemic Cell Death in Immature Oligodendrocytes: A Fatal Glutamate Release Feedback Loop [J]. J Neurosci, 2000, 20 (1): 34-42.
[130] BARGER SW, GOODWIN ME, PORTER MM, et al. Glutamate release from activated microglia requires the oxidative burst and lipid peroxidation [J]. Journal of Neurochemistry, 2007, 101 (5): 1205-1213.
[131] DOMERCQ M, SANCHEZ-GOMEZ MV, SHERWIN C, et al. System xc- and Glutamate Transporter Inhibition Mediates Microglial Toxicity to Oligodendrocytes [J]. J Immunol, 2007, 178 (10): 6549-6556.
[132] MATUTE C, ALBERDI E, IBARRETXE G, et al. Excitotoxicity in glial cells [J]. European Journal of Pharmacology, 2002, 447 (2-3): 239-246.
[133] DENG W, YUE Q, ROSENBERG PA, et al. Oligodendrocyte excitotoxicity determined by local glutamate accumulation and mitochondrial function [J]. Journal of Neurochemistry, 2006, 98 (1): 213-222.
[134] ALBERDI E, SANCHEZ-GOMEZ MV, TORRE I, et al. Activation of Kainate Receptors Sensitizes Oligodendrocytes to Complement Attack [J]. J Neurosci, 2006, 26 (12): 3220-3228.
[135] LI S, STYS PK. Mechanisms of Ionotropic Glutamate Receptor-Mediated Excitotoxicity in Isolated Spinal Cord White Matter [J]. J Neurosci, 2000, 20 (3): 1190-1198.
[136] SáNCHEZ-GóMEZ MV, MATUTE C. AMPA and Kainate Receptors Each Mediate Excitotoxicity in Oligodendroglial Cultures [J]. Neurobiology of Disease, 1999, 6 (6): 475-485.
[137] TANAKA H, GROOMS SY, BENNETT MVL, et al. The AMPAR subunit GluR2: still front and center-stage [J]. Brain Research, 2000, 886 (1-2): 190-207.
[138] HISAHARA S, SHOJI SI, OKANO H. ICE/CED-3 Family Executes Oligo- dendrocyte Apoptosis by Tumor Necrosis Factor [J]. Journal of Neurochemistry, 1997, 69 (1): 10-20.
[139] CURATOLO L, VALSASINA B, CACCIA C, et al. Recombinant human IL-2 is cytotoxic to oligodendrocytes after in vitro self aggregation [J]. Cytokine, 1997, 9 (10): 734-739.
[140] JUREWICZ A, MATYSIAK M, TYBOR K, et al. Tumour necrosis factor-induced death of adult human oligodendrocytes is mediated by apoptosis inducing factor [J]. Brain, 2005, 128 (11): 2675-2688.
[141] MERRILL, SCOLDING. Mechanisms of damage to myelin and oligodendro- cytes and their relevance to disease [J]. Neuropathology & Applied Neurobiology, 1999, 25 (6): 435-458.
[142] BELKA C, BUDACH W, KORTMANN RD, et al. Radiation induced CNS toxicity--molecular and cellular mechanisms [J]. Br J Cancer, 2001, 85 (9): 1233-1239.
[143] KURITA H, KAWAHARA N, ASAI A, et al. Radiation-induced apoptosis of oligodendrocytes in the adult rat brain [J]. Neurol Res, 2001, 23 (8): 869-874.
[144] HAQ E, GIRI S, SINGH I, et al. Molecular mechanism of psychosine induced cell death in human oligodendrocyte cell line [J]. Journal of Neurochemistry, 2003, 86 (6): 1428-1440.
[145] KHAN M, HAQ E, GIRI S, et al. Peroxisomal participation in psychosine mediated toxicity: Implications for Krabbe's disease [J]. Journal of Neuroscience Research, 2005, 80 (6): 845-854.
[146] GIRI S, KHAN M, RATTAN R, et al. Krabbe disease: psychosine-mediated activation of phospholipase A2 in oligodendrocyte cell death [J]. J Lipid Res, 2006, 47 (7): 1478-1492.
[147] JUNG M, SOMMER I, SCHACHNER M, et al. Monoclonal Antibody O10 Defines a Conformationally Sensitive Cell-Surface Epitope of Proteolipid Protein (PLP): Evidence that PLP Misfolding Underlies Dysmyelination in Mutant Mice [J]. J Neurosci, 1996, 16 (24): 7920-7929.
[148] PAK K, CHAN S, MATTSON M. Presenilin-1 mutation sensitizes oligoden-drocytes to glutamate and amyloid toxicities, and exacerbates white matter damage and memory impairment in mice [J]. NeuroMolecular Medicine, 2003, 3 (1): 53-64.
[149] QUINLAN RA, BRENNER M, GOLDMAN JE, et al. GFAP and its role in Alexander disease [J]. Experimental Cell Research, 2007, 313 (10): 2077-2087.
[150] MIGNOT C, BOESPFLUG-TANGUY O, GELOT A, et al. Alexander disease: putative mechanisms of an astrocytic encephalopathy [J]. Cellular and Molecular Life Sciences, 2004, 61 (3): 369-385.
[151] MOSER H, DUBEY P, FATEMI A. Progress in X-linked adrenoleuko- dystrophy [J]. Curr Opin Neurol, 2004, 17 (3): 263-269.
[152] Feigenbaum V, Gélot A, Casanova P, et al. Apoptosis in the Central Nervous System of Cerebral Adrenoleukodystrophy Patients [J]. Neurobiology of Disease, 2000, 7 (6): 600-612.
[153] ITO M, BLUMBERG B, MOCK D, et al. Potential environmental and host participants in the early white matter lesion of adreno-leukodystrophy: morphologic evidence for CD8 cytotoxic T cells, cytolysis of oligodendrocytes, and CD1-mediated lipid antigen presentation [J]. J Neuropathol Exp Neurol, 2001, 60 (10): 1004-1019.
[154] ARNETT H, MASON J, MARINO M, et al. TNF alpha promotes proliferation of oligodendrocyte progenitors and remyelination [J]. Nat Neurosci, 2001, 4 (11): 1116-1122.
[155] MASON JL, SUZUKI K, CHAPLIN DD, et al. Interleukin-1{beta} Promotes Repair of the CNS [J]. J Neurosci, 2001, 21 (18): 7046-7052.
[156] LOUIS J, MAGAL E, MUIR D, et al. CG-4, a new bipotential glial cell line from rat brain, is capable of differentiating in vitro into either mature oligodendrocytes or type-2 astrocytes [J]. J Neurosci Res, 1992, 31 (1): 193-204.
[157] NGUYEN D, H?PFNER M, ZOBEL F, et al. Rat oligodendroglial cell lines express a functional receptor for the chemokine CCL3 (macrophage inflammatory protein-1alpha) [J]. Neuroscience Letters, 2003, 351 (2): 71-74.
[158] YAO S, PANDEY P, LJUNGGREN-ROSE A, et al. LPS mediated injury to oligodendrocytes is mediated by the activation of nNOS: relevance to human demyelinating disease [J]. Nitric Oxide, 2010, 22 (3): 197-204.
[159] BARNETT M, PRINEAS J. Relapsing and remitting multiple sclerosis:pathology of the newly forming lesion [J]. Ann Neurol, 2004, 55 (4): 458-468.
[160] COMPSTON A, COLES A. Multiple sclerosis [J]. The Lancet, 2008, 372 (9648): 1502-1517.
[161] BRüCK W. The pathology of multiple sclerosis is the result of focal inflammatory demyelination with axonal damage [J]. Journal of Neurology, 2005, 252 (0): v3-v9.
[162] FREEDMAN R. Schizophrenia [J]. N Engl J Med, 2003, 349 (18): 1738-1749.
[163] SAWA A, SNYDER S. Schizophrenia: diverse approaches to a complex disease [J]. Science, 2003, 296 (5568): 692-695.
[164] MARTINS-DE-SOUZA D. Proteome and transcriptome analysis suggests oligodendrocyte dysfunction in schizophrenia [J]. J Psychiatr Res, 2010, 44 (3): 149-156.
[165] PRICE G, CERCIGNANI M, CHU EM, et al. Brain pathology in first episode psychosis: Magnetization transfer imaging provides additional information to MRI measurements of volume loss [J]. NeuroImage, 2010, 49 (1): 185-192.
[166] KUBICKI M, PARK H, WESTIN CF, et al. DTI and MTR abnormalities in schizophrenia: Analysis of white matter integrity [J]. NeuroImage, 2005, 26 (4): 1109-1118.
[167] URANOVA N, ORLOVSKAYA D, VIKHREVA O, et al. Electron microscopy of oligodendroglia in severe mental illness [J]. Brain Research Bulletin, 2001, 55 (5): 597-610.
[168] SCHMITT A, WILCZEK K, BLENNOW K, et al. Altered thalamic membrane phospholipids in schizophrenia: a postmortem study [J]. Biological Psychiatry, 2004, 56 (1): 41-45.
[169] LIU X, QIN W, HE G, et al. A family-based association study of the MOG gene with schizophrenia in the Chinese population [J]. Schizophrenia Research, 2005, 73 (2-3): 275-280.
[170] HOF PR, HAROUTUNIAN V, FRIEDRICH VL, et al. Loss and altered spatial distribution of oligodendrocytes in the superior frontal gyrus in schizophrenia [J]. Biological Psychiatry, 2003, 53 (12): 1075-1085.
[171] KAROUTZOU G, EMRICH HM, DIETRICH DE. The myelin-pathogenesis puzzle in schizophrenia: a literature review [J]. Mol Psychiatry, 2008, 13 (3): 245-260.
[172] MALBERG JE, EISCH AJ, NESTLER EJ, et al. Chronic AntidepressantTreatment Increases Neurogenesis in Adult Rat Hippocampus [J]. J Neurosci, 2000, 20 (24): 9104-9110.
[173] DUMAN RS, MALBERG J, NAKAGAWA S, et al. Neuronal plasticity and survival in mood disorders [J]. Biological Psychiatry, 2000, 48 (8): 732-739.
[174] SANTARELLI L, SAXE M, GROSS C, et al. Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants [J]. Science, 2003, 301 (5634): 805-809.
[175] MALBERG JE, DUMAN RS. Cell Proliferation in Adult Hippocampus is Decreased by Inescapable Stress: Reversal by Fluoxetine Treatment [J]. Neuropsychopharmacology, 2003, 28 (9): 1562-1571.
[176] WAKADE CG, MAHADIK SP, WALLER JL, et al. Atypical neuroleptics stimulate neurogenesis in adult rat brain [J]. Journal of Neuroscience Research, 2002, 69 (1): 72-79.
[177] HALIM ND, WEICKERT CS, MCCLINTOCK BW, et al. Effects of Chronic Haloperidol and Clozapine Treatment on Neurogenesis in the Adult Rat Hippocampus [J]. Neuropsychopharmacology, 2004, 29 (6): 1063-1069.
[178] SCHMITT A, WEBER S, JATZKO A, et al. Hippocampal volume and cell proliferation after acute and chronic clozapine or haloperidol treatment [J]. Journal of Neural Transmission, 2004, 111 (1): 91-100.
[179] WANG H-D, DUNNAVANT FD, JARMAN T, et al. Effects of Antipsychotic Drugs on Neurogenesis in the Forebrain of the Adult Rat [J]. Neuropsychopharmacology, 2004, 29 (7): 1230-1238.
[180] KIPPIN TE, KAPUR S, VAN DER KOOY D. Dopamine Specifically Inhibits Forebrain Neural Stem Cell Proliferation, Suggesting a Novel Effect of Antipsychotic Drugs [J]. J Neurosci, 2005, 25 (24): 5815-5823.
[181] VOSTRIKOV VM, URANOVA NA, ORLOVSKAYA DD. Deficit of perineuronal oligodendrocytes in the prefrontal cortex in schizophrenia and mood disorders [J]. Schizophrenia Research, 2007, 94 (1-3): 273-280.
[182] HAROUTUNIAN V, KATSEL P, DRACHEVA S, et al. Variations in oligodendrocyte- related gene expression across multiple cortical regions: implications for the pathophysiology of schizophrenia [J]. The International Journal of Neuropsychopharmacology, 2007, 10 (04): 565-573.
[183] MIMMACK M, RYAN M, BABA H, et al. Gene expression analysis in schizophrenia: reproducible up-regulation of several members of theapolipoprotein L family located in a high-susceptibility locus for schizophrenia on chromosome 22 [J]. Proc Natl Acad Sci U S A, 2002, 99 (7): 4680-4685.
[184] SANFILIPO M, LAFARGUE T, ARENA L, et al. Fine Volumetric Analysis of the Cerebral Ventricular System in Schizophrenia: Further Evidence for Multifocal Mild to Moderate Enlargement [J]. Schizophr Bull, 2000, 26 (1): 201-216.
[185] SIGMUNDSSON T, SUCKLING J, MAIER M, et al. Structural Abnormalities in Frontal, Temporal, and Limbic Regions and Interconnecting White Matter Tracts in Schizophrenic Patients With Prominent Negative Symptoms [J]. Am J Psychiatry, 2001, 158 (2): 234-243.
[186] BAGARY MS, SYMMS MR, BARKER GJ, et al. Gray and White Matter Brain Abnormalities in First-Episode Schizophrenia Inferred From Magneti- zation Transfer Imaging [J]. Arch Gen Psychiatry, 2003, 60 (8): 779-788.
[187] MATSUSHIMA GK, MORELL P. The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system. [J]. Brain Pathol, 2001, 1 (11): 107-116.
[188] KOMOLY S. Experimental demyelination caused by primary oligoden- drocyte dystrophy. Regional distribution of the lesions in the nervous system of mice [J]. Ideggyogy Sz, 2005, 58 (1-2): 40-43.
[189] HUILLARD E, ROWITCH DH. Olig2 function in adult neural stem and progenitor cells [J]. International Journal of Developmental Neuroscience, 2008, 26 (8): 872-872.
[190] HUANG K, TANG W, TANG R, et al. Positive association between OLIG2 and schizophrenia in the Chinese Han population [J]. Human Genetics, 2008, 122 (6): 659-660.
[191] LI H, LU Y, SMITH H, et al. Olig1 and Sox10 interact synergistically to drive myelin basic protein transcription in oligodendrocytes [J]. The Journal of Neuroscience, 2007 27 (52): 14375-14382.
[192] ZHOU Q, ANDERSON DJ. The bHLH Transcription Factors OLIG2 and OLIG1 Couple Neuronal and Glial Subtype Specification [J]. Cell, 2002, 109 (1): 61-73.
[193] HALL AK, MILLER RH. Emerging roles for bone morphogenetic proteins in central nervous system glial biology [J]. Journal of Neuroscience Research, 2004, 76 (1): 1-8.
[194] AGIUS E, SOUKKARIEH C, DANESIN C, et al. Converse control of oligodendrocyte and astrocyte lineage development by Sonic hedgehog in the chick spinal cord [J]. Developmental Biology, 2004, 270 (2): 308-321.
[195] GOMES WA, MEHLER MF, KESSLER JA. Transgenic overexpression of BMP4 increases astroglial and decreases oligodendroglial lineage commitment [J]. Developmental Biology, 2003, 255 (1): 164-177.
[196] CHENG X, WANG Y, HE Q, et al. Bone Morphogenetic Protein Signaling and Olig1/2 Interact to Regulate the Differentiation and Maturation of Adult Oligodendrocyte Precursor Cells [J]. Stem Cells, 2007, 25 (12): 3204-3214.
[197] ONO K, TAKEBAYASHI H, IKEDA K, et al. Regional- and temporal dependent changes in the differentiation of Olig2 progenitors in the forebrain, and the impact on astrocyte development in the dorsal pallium [J]. Developmental Biology, 2008, 320 (2): 456-468.
[198] KOUKO TATSUMI, TAKEBAYASHI H, MANABE T, et al. Genetic fate mapping of Olig2 progenitors in the injured adult cerebral cortex reveals preferential differentiation into astrocytes [J]. Journal of Neuroscience Research, 2008, 86 (16): 3494-3502.
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |