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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 賴文崧 | |
| dc.contributor.author | Ching-Hsun Huang | en |
| dc.contributor.author | 黃勁勳 | zh_TW |
| dc.date.accessioned | 2021-06-16T03:44:26Z | - |
| dc.date.available | 2016-03-13 | |
| dc.date.copyright | 2015-03-13 | |
| dc.date.issued | 2015 | |
| dc.date.submitted | 2015-02-09 | |
| dc.identifier.citation | Addington, J., & Addington, D. (1999). Neurocognitive and social functioning in schizophrenia. Schizophr Bull, 25(1), 173-182.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/55016 | - |
| dc.description.abstract | 從人類遺傳學累積的研究證據顯示有若干候選基因可能對於思覺失調症的病因有著重要的影響，包含AKT1 及NRG1。最近的研究也指出，經由NRG1刺激ErbB2/4接受器活化PI3K/AKT 訊息傳導，在思覺失調症的行為缺損中扮演著重要的角色。善用基因剃除小鼠的研究模式，可以直接檢驗Akt1/Nrg1基因單獨及雙重變異小鼠還有它們的同窩野生控制組小鼠之間的差異，進而用來探討Akt1/Nrg1基因之間的交互作用對於認知行為及社會行為的影響。本研究共包含三個主要的實驗。在實驗一中，研究發現，基因雙重變異小鼠體重與其他三組沒有明顯差異。然而，Akt1基因單獨變異及雙重變異的小鼠在紋狀體及背側海馬迴這兩個腦區，則表現出比較低的腦部活動。在實驗二中，小鼠基本行為的檢測結果並未發現有任何明顯地基因變異所造成的影響，包含自發性運動行為、類焦慮行為以及感覺動作反射。在認知行為作業中，則發現Nrg1基因單獨變異及雙重變異的小鼠，會表現出類事件記憶的缺損。在社會行為測試中，只發現有基因雙重變異的小鼠會表現出明顯地社交畏縮的行為。實驗三中，Akt1/Nrg1基因之間的協同作用則進一步在基因雙重變異的小鼠身上得到確認。特別是它們在與成年雄性之間以及與卵巢切除母鼠間的互動，都表現出明顯地社交畏縮行為。另一方面，Nrg1基因單獨變異及雙重變異的小鼠，在母鼠尿液刺激下，則發出比較少的超聲波。總結來說，本研究的實驗結果揭露了Akt1/Nrg1基因的雙重變異對於社會認知功能的影響，而這樣的影響可能是造成思覺失調症相關的社會功能缺損的病因之一。 | zh_TW |
| dc.description.abstract | An accumulation of evidence from human genetic studies has suggested several functional candidate genes for the susceptibility to schizophrenia, including AKT1 and neuregulin 1 (NRG1). Recent findings also revealed that NRG1 acts through ErbB2/4 in a paracrine fashion to stimulate the PI3-kinase/AKT signaling pathway, which might be involved in the functional deficiencies of the schizophrenic. To build our model, we controlled and bred Akt1/Nrg1 single and double mutant mice and their wild-type littermate controls. We used these mice to examine the epistasis effect of Nrg1 and Akt1 on the regulation of behavioral phenotypes, cognition, and social functions. We conducted a set of three experiments in this study. In Experiment 1, double mutant mice displayed a normal profile of bodyweight during development, whereas Akt1+/- and double mutant mice displayed lower brain activity in the striatum and dorsal hippocampus, as per microPET scan results. In Experiment 2, we found no significant genotypic differences in our basic behavioral phenotying, including locomotion, anxiety-like behavior, and sensorimotor gating. However, both double mutant mice and Nrg1+/- mice exhibited impaired episodic-like memory. Double mutant mice also had impaired sociability. In Experiment 3, a synergistic epistasis between Akt1 and Nrg1 was further confirmed in double mutant mice in that they had impaired social interaction compared to the other three groups, a result especially significant when these mice encountered a novel male or an ovariectomized female. Double mutant mice and Nrg1+/- mice also emitted fewer female urine-induced ultrasonic vocalization calls. Collectively, our results indicate that double deficiency of Akt1 and Nrg1 can result in the impairment of social cognitive functions, which might be pertinent to the pathogenesis of schizophrenia-related social cognitions. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T03:44:26Z (GMT). No. of bitstreams: 1 ntu-104-D96227106-1.pdf: 6342286 bytes, checksum: 75e4cbe038c087e673f1a19e8e6d9740 (MD5) Previous issue date: 2015 | en |
| dc.description.tableofcontents | Table of contents
Chapter 1. General introduction 1 1. What is schizophrenia? 1 1.1 The symptoms of schizophrenia 2 1.2 Cognitive/social impairments as the core symptoms of schizophrenia 3 2. Etiology of schizophrenia 5 2.1 The environmental risks for schizophrenia 5 2.2 The genetic risk factors of schizophrenia 7 2.3 AKT1 as a candidate gene of schizophrenia 8 2.3.1 What is AKT1? 8 2.3.2 AKT1 and schizophrenia 10 2.4 NRG1 as a candidate gene of schizophrenia 11 2.4.1 What is NRG1? 11 2.4.2 NRG1 and schizophrenia 13 3. Modeling schizophrenia in genetically engineered mice 15 3.1 The Akt1-deficient mouse model of schizophrenia 16 3.2 The Nrg1-deficient mouse model of schizophrenia 18 4. NRG1-induced AKT1 phosphorylation: a potential biomarker of schizophrenia 21 5. Study objectives 23 Chapter 2. Materials and Methods 25 1. Animals 25 2. Experiment 1: General features of Akt1-Nrg1 single and double mutant mice 27 2.1 Physical growth: 27 2.2 The expression of Akt1 and Nrg1 proteins in the cerebral cortex: 27 2.3 The measurement of basic brain activity using MicroPET scans: 28 3. Experiment 2.1: Basic behavioral phenotyping of Akt1-Nrg1 single and double mutant mice 30 3.1 Locomotion activity: 30 3.2 Elevated plus maze: 31 3.3 Pre-pulse inhibition: 31 4. Experiment 2.2: Evaluation of cognitive and social functions in Akt1-Nrg1 single and double mutant mice 33 4.1 Episodic-like memory: 33 4.2 Sociability and social recognition: 34 4.3 Working memory: 36 5. Experiment 3: Examination of social interactions and social communication in Akt1-Nrg1 single and double mutant mice 38 5.1 Estrus determination by vaginal smear and urine collection in mice 38 5.2 Previous estrus female experiences 39 5.3 Experimental procedure 40 6. Statistical analysis 41 Chapter 3. The results 43 1. Experiment 1: General features of Akt1-Nrg1 single and double mutant mice 43 2. Experiment 2.1: Basic behavioral phenotyping 44 3. Experiment 2.2: Evaluation of cognitive and social functions 45 4. Experiment 3: Social interaction and social communication 46 Chapter 4. Discussion 49 1. Summary of the results 49 2. Potential targeted brain regions and neurotransmitter systems of Akt1-Nrg1 epistatic effects 50 3. Cognitive deficits in Akt1-Nrg1 single and double mutant mice 52 4. Social cognition deficits in Akt1-Nrg1 single and double mutant mice 55 4.1 The synergistic effect of Akt1 and Nrg1 on sociability 57 4.2 Asynthetic epistasis of Akt1 and Nrg1 on social recognition 58 4.3 Reduction of female urine induced USV in Nrg1+/- and double mutant mice 60 5. Contributions and applications 62 References 111 Appendix…….………………………………………………………………………….138 Figures and Table Figure 1. The schematic diagram of the Akt1 targeting strategy. 65 Figure 2. The schematic diagram of the Nrg1 targeting strategy. 67 Figure 3. The regions of interest in mouse brain atlases 69 Figure 4. A schematic drawing of the “what,” “where,” and “when” object exploration task. 71 Figure 5. A schematic drawing of sociability and social recognition. 73 Figure 6. Vaginal cytology representing each stage of the estrous cycle. 75 Figure 7. The flow chart and apparatus of social interaction and social communication. 77 Figure 8. Physical growth measurement represented by body weight.. 79 Figure 9. Expression of cerebral Akt1 protein levels in wild type, Akt1+/-, Nrg1+/-, and double mutant mice. 81 Figure 10. Expression of cerebral Nrg1 protein levels in wild type, Akt1+/-, Nrg1+/-, and double mutant mice. 83 Figure 11. Examination of basic brain activity in the medial prefrontal cortex 85 Figure 12. Representative PET-CT fusion images of coronal slices 87 Figure 13. Examination of basic brain activity in each sub-region of the striatum 89 Figure 14. Representative PET-CT fusion images of coronal slices 91 Figure 15. Examination of basic brain activity in the dorsal and ventral hippocampus 93 Figure 16. The spontaneous locomotor activity 95 Figure 17. Anxiety-like behavior 97 Figure 18. The percentages of pre-pulse inhibition 99 Figure 19. The episodic-like memory performance 101 Figure 20. Total sniffing time of wild-type, Akt1+/-, Nrg1+/-, and double mutant mice in the sociability and social recognition tasks of Experiment 2 103 Figure 21. The accuracy of working memory 105 Figure 22. Total sniffing time and number of calls of wild-type, Akt1+/-, Nrg1+/-, and double mutant mice in the social interaction and social communication task in Experiment 3. 107 Table1. A summary of epistatic effects in general features, basic behaviors, cognitive functions, and social cognitive functions. 109 | |
| dc.language.iso | en | |
| dc.subject | 基因交互作用 | zh_TW |
| dc.subject | 小鼠行為作業 | zh_TW |
| dc.subject | Akt1 | zh_TW |
| dc.subject | 小鼠社會行為 | zh_TW |
| dc.subject | Nrg1 | zh_TW |
| dc.subject | 基因雙重剃除小鼠 | zh_TW |
| dc.subject | 思覺失調症 | zh_TW |
| dc.subject | social communication | en |
| dc.subject | Akt1 | en |
| dc.subject | neuregulin 1 (Nrg1) | en |
| dc.subject | double mutant mice | en |
| dc.subject | schizophrenia | en |
| dc.subject | epistatic effect | en |
| dc.subject | behavioral phenotyping | en |
| dc.subject | social interaction | en |
| dc.title | 思覺失調症候選基因Akt1與neuregulin 1的交互作用
對於小鼠社會行為的影響 | zh_TW |
| dc.title | The epistatic effect between Akt1 and neuregulin 1 on the regulation of behavioral phenotypes and social functions in genetic mouse models of schizophrenia. | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 103-1 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 梁庚辰,劉怡均,劉智民,廖文霖,陳志成 | |
| dc.subject.keyword | Akt1,Nrg1,基因雙重剃除小鼠,思覺失調症,基因交互作用,小鼠行為作業,小鼠社會行為, | zh_TW |
| dc.subject.keyword | Akt1,neuregulin 1 (Nrg1),double mutant mice,schizophrenia,epistatic effect,behavioral phenotyping,social interaction,social communication, | en |
| dc.relation.page | 157 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2015-02-09 | |
| dc.contributor.author-college | 理學院 | zh_TW |
| dc.contributor.author-dept | 心理學研究所 | zh_TW |
| 顯示於系所單位： | 心理學系 | |
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