探討剔除Dtnbp1基因對於公和母鼠前額葉多巴胺傳遞路徑與社交行為的影響

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潘瑋婷(Wei-Ting Pan) 查詢紙本館藏

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探討剔除Dtnbp1基因對於公和母鼠前額葉多巴胺傳遞路徑與社交行為的影響
(Investigate dopamine signaling in the prefrontal cortex and social behavior in sex-dependent Dtnbp1 mutant mice)

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至系統瀏覽論文 (2027-6-30以後開放)

摘要(中)

Dtnbp1 (dystrobrevin-binding protein 1 gene) 是一種與思覺失調症相關的遺傳因子。過去的文獻證實，剔除Dtnbp1 (Dys-/-) 會減弱小鼠記憶，包含工作記憶、恐懼記憶以及識別記憶，然而，很少有研究探討剔除Dtnbp1公鼠和母鼠對思覺失調症其一症狀-社交行為的影響。本篇研究結果顯示，Dys-/- 公鼠的社會階級較低於對照組wild-type (WT) 公鼠，反之，Dys-/- 母鼠的社交階級則較高於對照組WT母鼠。此外，Dys-/- 母鼠展現社交行為障礙，而Dys-/- 公鼠則無此行為缺陷。這些研究結果顯示Dtnbp1 gene會參與社交行為的表徵且存在性別上的差異。社交行為受大腦前額葉皮質區 (prefrontal cortex) 高度調控，因此針對Dys-/- 小鼠前額葉皮質進行分子及訊息傳遞路徑分析後，發現與對照組相比，Dys-/- 公鼠與母鼠的Activity-regulated cytoskeleton-associated protein (Arc) 蛋白皆顯著減少，Calcium/calmodulin-dependent protein kinase II (CaMKII) 活性在Dys-/- 公鼠也顯著減少，但在Dys-/- 母鼠中則沒有顯著差異。此外，在Dys-/- 公鼠前額葉皮質發現多巴胺Drd3受體mRNA表達顯著上升，然在Dys-/-母鼠前額葉皮質中則發現多巴胺Drd1以及Drd2受體mRNA表達水平下降，進一步分析Dys-/- 母鼠前額葉皮質多巴胺Drd2受體下游訊息傳遞路徑，發現GSK3β活性顯著降低。當Dys-/- 母鼠以管餵餵食多巴胺Drd2受體激動劑的抗精神病藥物銳思定膜衣錠 (brexpiprazole) 14天後，這些小鼠有改善社交行為之趨勢。綜合上述結果顯示Dtnbp1參與調控多巴胺神經途徑以及影響小鼠社交行為能力，也為治療思覺失調症提供新的見解。

摘要(英)

The dystrobrevin-binding protein 1 gene (Dtnbp1) has been identified as one of genes associated with schizophrenia. Previous studies have demonstrated that working memory、fear and recognition memory were damaged in Dys-/- mice. However, there is no studies exploring whether mutation of Dtnbp1 in male and female mice exhibit deficits in social behavior since social dysfunction is one of pathologoical hallmarks seen in patients with schizophrenia. The current study showed that dominance hierarchy differed in both male and female Dys-/- mice compared with their wild-type (WT) littermate. Additionally, female Dys-/- mice were unable to recognize new partner versus old partner in three chamber social interaction test, while male Dys-/- exhibited preferred to interact with new partener in such test. These results indicated that Dtnbp1 gene is involved in sex-specific social behavior. At the cellular level, male and female Dys-/- shared common and distinct cellular signaling in the medial prefrontal cortex (mPFC), a brain region that is critical for social behavior. Specifically, both activity-regulated cytoskeleton-associated protein (Arc) protein expression and calcium/calmodulin-dependent protein kinase II (CaMKII) activity were downregulated in the mPFC of male Dys-/- mice compared wht WT littermate. However, Arc level, but not CaMKII activity, in the mPFC was decreased only in female Dys-/- mice compared to their WT littermate. At the molecular level, dopamine receptor D3 (Drd3) was the only type of dopamine receptors diminished in the mPFC of male Dys-/-mice. Interesting, dopamine receptor D1 and D2 (Drd1, Drd2) in the mPFC were both reduced in female Dys-/- mice compared with WT mice. The decrease in Drd2 expression in the mPFC was in corresponding to downregulation of GSK3β activity in female Dys-/- mice. Lastly, treatment with the antipsycotic brexpiprazole in female Dys-/- mice for 14 days showed a trend toward an increase in social interaction. Taken together, the results suggested that Dtnbp1 gene is involved in regulating dopamine signaling, which ultimately influences social behavior. This study provides a new insight into therapeutic approach in treating schizophrenia.

關鍵字(中)

★ 思覺失調症
★ 前額葉皮質區
★ 多巴胺
★ 銳思定膜衣錠

關鍵字(英)

★ Schizophrenia
★ dystrobrevin-binding protein 1
★ dopamine
★ brexpiprazole

論文目次

中文摘要 i
英文摘要 Abstract ii
誌謝 iii
目錄 iv
圖目錄 vi
表目錄 vii
中英文對照表 viii
一、緒論 1
1-1 思覺失調症 1
1-2 社會行為 1
1-3 前額葉皮質區調控社會行為 3
1-4 Dystrobrevin-binding protein 1 gene(Dtnbp1)與思覺失調症之關聯 6
1-5 Dysbindin-1蛋白的功能 7
1-6 Dtnbp1突變小鼠-行為上的改變 8
1-7 Dtnbp1突變小鼠-細胞及分子層次的改變 10
1-8 多巴胺(Dopamine)系統 12
1-9 抗精神病藥Brexpiprazole 14
1-10 研究動機與目的 15
二、研究方法及材料 16
2-1 實驗動物 16
2-2 聚合酶連鎖反應 16
2-3 曠野實驗 16
2-4 管型社會支配實驗 17
2-5 三隔間社交行為 17
2-6 社交傳遞的食物偏好行為 18
2-7 Brexpiprazole藥物投予 19
2-8 犧牲實驗小鼠 19
2-9 西式點墨法 19
2-10 即時聚合酶連鎖反應 20
2-11 統計分析 21
三、實驗結果 22
3-1 鑑定子代小鼠的基因型，證實小鼠的Dtnbp1基因被完全消除 22
3-2 消除Dtnbp1對於公和母鼠運動能力以及焦慮表現之影響 22
3-3 WT和Dys-/-小鼠的社會階級表徵展現性別差異性 23
3-4 Dys-/-母鼠具有正常的社交能力，但缺乏社交識別能力 23
3-5 Dys-/-公鼠的社交傳遞嗅覺行為維持正常的功能 24
3-6 Dysbindin-1蛋白下降改變小鼠前額葉皮質區中CaMKIIα以及Arc蛋白表達量 25
3-7 Dys-/-小鼠前額葉皮質區中多巴胺受體的表達量異常 26
3-8 Dys-/-小鼠前額葉皮質區中磷酸化GSK3β表達量增加 26
3-9 Brexpiprazole具改善Dys-/-母鼠社交障礙之潛在性 27
四、討論 29
五、結論 33
參考文獻 44
附錄 53

參考文獻

1. Lewis, D.A. and J.A. Lieberman, Catching up on schizophrenia: natural history and neurobiology. Neuron, 2000. 28(2): p. 325-334.
2. Kessler, R.C., et al., Age of onset of mental disorders: a review of recent literature. Current opinion in psychiatry, 2007. 20(4): p. 359.
3. Robinson, N. and S.E. Bergen, Environmental risk factors for schizophrenia and bipolar disorder and their relationship to genetic risk: Current knowledge and future directions. Frontiers in Genetics, 2021. 12: p. 999.
4. Hilker, R., et al., Heritability of schizophrenia and schizophrenia spectrum based on the nationwide Danish twin register. Biological psychiatry, 2018. 83(6): p. 492-498.
5. Van Os, J., G. Kenis, and B.P. Rutten, The environment and schizophrenia. Nature, 2010. 468(7321): p. 203-212.
6. Green, M.F., W.P. Horan, and J. Lee, Social cognition in schizophrenia. Nature Reviews Neuroscience, 2015. 16(10): p. 620-631.
7. Green, M.F., et al., Social disconnection in schizophrenia and the general community. Schizophrenia bulletin, 2018. 44(2): p. 242-249.
8. Corradi-Dell′Acqua, C., et al., What determines social behavior? Investigating the role of emotions, self-centered motives, and social norms. Frontiers in Human Neuroscience, 2016. 10: p. 342.
9. Wang, F., et al., Bidirectional control of social hierarchy by synaptic efficacy in medial prefrontal cortex. Science, 2011. 334(6056): p. 693-697.
10. Ferreira-Fernandes, E. and J. Peça, The Neural Circuit Architecture of Social Hierarchy in Rodents and Primates. Frontiers in Cellular Neuroscience, 2022: p. 192.
11. Wang, Y., et al., Accelerated evolution of an Lhx2 enhancer shapes mammalian social hierarchies. Cell research, 2020. 30(5): p. 408-420.
12. Franco, L.O., et al., Social subordination induced by early life adversity rewires inhibitory control of the prefrontal cortex via enhanced Npy1r signaling. Neuropsychopharmacology, 2020. 45(9): p. 1438-1447.
13. Wei, D., V. Talwar, and D. Lin, Neural circuits of social behaviors: innate yet flexible. Neuron, 2021. 109(10): p. 1600-1620.
14. Wesson, D.W., Sniffing behavior communicates social hierarchy. Current Biology, 2013. 23(7): p. 575-580.
15. Grossmann, T., Mapping prefrontal cortex functions in human infancy. Infancy, 2013. 18(3): p. 303-324.
16. Wood, J.N. and J. Grafman, Human prefrontal cortex: processing and representational perspectives. Nature reviews neuroscience, 2003. 4(2): p. 139-147.
17. Bicks, L.K., et al., Prefrontal cortex and social cognition in mouse and man. Frontiers in psychology, 2015. 6: p. 1805.
18. Shepherd, G.M., The microcircuit concept applied to cortical evolution: from three-layer to six-layer cortex. Frontiers in neuroanatomy, 2011. 5: p. 30.
19. Thomson, A.M. and C. Lamy, Functional maps of neocortical local circuitry. Frontiers in neuroscience, 2007: p. 2.
20. Anderson, S.W., et al., Impairment of Social and Moral Behavior Related to Early Damage in Human Prefrontal Cortek, in Social neuroscience. 2013, Psychology Press. p. 29-39.
21. Krienen, F.M., P.-C. Tu, and R.L. Buckner, Clan mentality: evidence that the medial prefrontal cortex responds to close others. Journal of Neuroscience, 2010. 30(41): p. 13906-13915.
22. Lee, E., et al., Enhanced neuronal activity in the medial prefrontal cortex during social approach behavior. Journal of Neuroscience, 2016. 36(26): p. 6926-6936.
23. Xu, S., et al., Neural Circuits for Social Interactions: From Microcircuits to Input-Output Circuits. Frontiers in Neural Circuits, 2021: p. 126.
24. Huang, W.-C., et al., Social behavior is modulated by valence-encoding mPFC-amygdala sub-circuitry. Cell reports, 2020. 32(2): p. 107899.
25. Yizhar, O., et al., Neocortical excitation/inhibition balance in information processing and social dysfunction. Nature, 2011. 477(7363): p. 171-178.
26. Felix-Ortiz, A.C., et al., Bidirectional modulation of anxiety-related and social behaviors by amygdala projections to the medial prefrontal cortex. Neuroscience, 2016. 321: p. 197-209.
27. Straub, R.E., et al., Genetic variation in the 6p22.3 gene DTNBP1, the human ortholog of the mouse dysbindin gene, is associated with schizophrenia. Am J Hum Genet, 2002. 71(2): p. 337-48.
28. Owen, M.J., N.M. Williams, and M.C. O′Donovan, The molecular genetics of schizophrenia: new findings promise new insights. Molecular psychiatry, 2004. 9(1): p. 14-27.
29. Talbot, K., et al., Dysbindin-1 is a synaptic and microtubular protein that binds brain snapin. Human molecular genetics, 2006. 15(20): p. 3041-3054.
30. Talbot, K., et al., Dysbindin-1 is reduced in intrinsic, glutamatergic terminals of the hippocampal formation in schizophrenia. J Clin Invest, 2004. 113(9): p. 1353-63.
31. Oyama, S., et al., Dysbindin-1, a schizophrenia-related protein, functionally interacts with the DNA-dependent protein kinase complex in an isoform-dependent manner. PLoS One, 2009. 4(1): p. e4199.
32. Talbot, K., et al., Handbook of neurochemistry and molecular neurobiology. 2009.
33. Benson, M.A., et al., Dysbindin, a novel coiled-coil-containing protein that interacts with the dystrobrevins in muscle and brain. Journal of Biological Chemistry, 2001. 276(26): p. 24232-24241.
34. Ito, H., et al., Dysbindin-1, WAVE2 and Abi-1 form a complex that regulates dendritic spine formation. Mol Psychiatry, 2010. 15(10): p. 976-86.
35. H.G., L., Localization of dystrophin to postsynaptic regions of central nervous system cortical neurons Nature 1990.
36. Blake, D.J., et al., Different dystrophin-like complexes are expressed in neurons and glia. The Journal of cell biology, 1999. 147(3): p. 645-658.
37. Ghiani, C., et al., The dysbindin-containing complex (BLOC-1) in brain: developmental regulation, interaction with SNARE proteins and role in neurite outgrowth. Molecular psychiatry, 2010. 15(2): p. 204-215.
38. Harris, J.J., R. Jolivet, and D. Attwell, Synaptic energy use and supply. Neuron, 2012. 75(5): p. 762-777.
39. Suh, B.K., et al., Schizophrenia-associated dysbindin modulates axonal mitochondrial movement in cooperation with p150glued. Molecular brain, 2021. 14(1): p. 1-14.
40. Zhao, J., et al., Dysbindin-1 regulates mitochondrial fission and gamma oscillations. Molecular psychiatry, 2021. 26(9): p. 4633-4651.
41. Huang, C.C., et al., Deletion of Dtnbp1 in mice impairs threat memory consolidation and is associated with enhanced inhibitory drive in the amygdala. Translational psychiatry, 2019. 9(1): p. 1-15.
42. Talbot, K., The sandy (sdy) mouse: a dysbindin-1 mutant relevant to schizophrenia research. 2009. 179: p. 87-94.
43. Hattori, S., et al., Behavioral abnormalities and dopamine reductions in sdy mutant mice with a deletion in Dtnbp1, a susceptibility gene for schizophrenia. Biochemical and biophysical research communications, 2008. 373(2): p. 298-302.
44. Petit, E.I., et al., Dysregulation of specialized delay/interference-dependent working memory following loss of dysbindin-1A in schizophrenia-related phenotypes. Neuropsychopharmacology, 2017. 42(6): p. 1349-1360.
45. Tang, J., et al., Dysbindin-1 in dorsolateral prefrontal cortex of schizophrenia cases is reduced in an isoform-specific manner unrelated to dysbindin-1 mRNA expression. Hum Mol Genet, 2009. 18(20): p. 3851-63.
46. Takao, K., et al., Impaired long-term memory retention and working memory in sdy mutant mice with a deletion in Dtnbp1, a susceptibility gene for schizophrenia. Molecular brain, 2008. 1(1): p. 1-12.
47. Chang, E., et al., Single point mutation on the gene encoding dysbindin results in recognition deficits. Genes, Brain and Behavior, 2018. 17(5): p. e12449.
48. Cox, M., et al., Neurobehavioral abnormalities in the dysbindin‐1 mutant, sandy, on a C57BL/6J genetic background. Genes, Brain and Behavior, 2009. 8(4): p. 390-397.
49. Feng, Y.-Q., et al., Dysbindin deficiency in sandy mice causes reduction of snapin and displays behaviors related to schizophrenia. Schizophrenia research, 2008. 106(2-3): p. 218-228.
50. Leggio, G., et al., The epistatic interaction between the dopamine D3 receptor and dysbindin-1 modulates higher-order cognitive functions in mice and humans. Molecular psychiatry, 2021. 26(4): p. 1272-1285.
51. Bhardwaj, S.K., et al., Behavioral characterization of dysbindin-1 deficient sandy mice. Behavioural brain research, 2009. 197(2): p. 435-441.
52. Glen Jr, W.B., et al., Dysbindin‐1 loss compromises NMDAR‐dependent synaptic plasticity and contextual fear conditioning. Hippocampus, 2014. 24(2): p. 204-213.
53. Li, W., et al., Hermansky-Pudlak syndrome type 7 (HPS-7) results from mutant dysbindin, a member of the biogenesis of lysosome-related organelles complex 1 (BLOC-1). Nature genetics, 2003. 35(1): p. 84-89.
54. Moghaddam, B., Bringing order to the glutamate chaos in schizophrenia. Neuron, 2003. 40(5): p. 881-884.
55. Tang, T.T.-T., et al., Dysbindin regulates hippocampal LTP by controlling NMDA receptor surface expression. Proceedings of the National Academy of Sciences, 2009. 106(50): p. 21395-21400.
56. Karlsgodt, K.H., et al., Reduced dysbindin expression mediates N-methyl-D-aspartate receptor hypofunction and impaired working memory performance. Biological psychiatry, 2011. 69(1): p. 28-34.
57. Papaleo, F., et al., Dysbindin-1 modulates prefrontal cortical activity and schizophrenia-like behaviors via dopamine/D2 pathways. Molecular psychiatry, 2012. 17(1): p. 85-98.
58. Zhou, Y., et al., Interactions between the NR2B receptor and CaMKII modulate synaptic plasticity and spatial learning. Journal of Neuroscience, 2007. 27(50): p. 13843-13853.
59. Bayer, K., et al., Interaction with the NMDA receptor locks CaMKII in an active conformation. Nature, 2001. 411(6839): p. 801-805.
60. Tovote, P., J.P. Fadok, and A. Lüthi, Neuronal circuits for fear and anxiety. Nature Reviews Neuroscience, 2015. 16(6): p. 317-331.
61. Plath, N., et al., Arc/Arg3. 1 is essential for the consolidation of synaptic plasticity and memories. Neuron, 2006. 52(3): p. 437-444.
62. Shepherd, J.D. and M.F. Bear, New views of Arc, a master regulator of synaptic plasticity. Nature neuroscience, 2011. 14(3): p. 279-284.
63. Ploski, J.E., et al., The activity-regulated cytoskeletal-associated protein (Arc/Arg3. 1) is required for memory consolidation of pavlovian fear conditioning in the lateral amygdala. Journal of Neuroscience, 2008. 28(47): p. 12383-12395.
64. Bramham, C.R., et al., The immediate early gene arc/arg3. 1: regulation, mechanisms, and function. Journal of Neuroscience, 2008. 28(46): p. 11760-11767.
65. Manago, F., et al., Genetic disruption of Arc/Arg3. 1 in mice causes alterations in dopamine and neurobehavioral phenotypes related to schizophrenia. Cell reports, 2016. 16(8): p. 2116-2128.
66. Yuan, Q., et al., Regulation of brain-derived neurotrophic factor exocytosis and gamma-aminobutyric acidergic interneuron synapse by the schizophrenia susceptibility gene dysbindin-1. Biological psychiatry, 2016. 80(4): p. 312-322.
67. Jia, J.-M., et al., The schizophrenia susceptibility gene dysbindin regulates dendritic spine dynamics. Journal of Neuroscience, 2014. 34(41): p. 13725-13736.
68. Kolluri, N., et al., Lamina-specific reductions in dendritic spine density in the prefrontal cortex of subjects with schizophrenia. American Journal of Psychiatry, 2005. 162(6): p. 1200-1202.
69. Klein, M.O., et al., Dopamine: Functions, Signaling, and Association with Neurological Diseases. Cell Mol Neurobiol, 2019. 39(1): p. 31-59.
70. Carlsson, Perspectives on the discovery of central monoaminergic neurotransmission. Annu Rev Neurosci, 1987. 10: p. 19-40.
71. Dal Toso, R., et al., The dopamine D2 receptor: two molecular forms generated by alternative splicing. The EMBO journal, 1989. 8(13): p. 4025-4034.
72. Giros, B., et al., Alternative splicing directs the expression of two D2 dopamine receptor isoforms. Nature, 1989. 342(6252): p. 923-926.
73. De Mei, C., et al., Getting specialized: presynaptic and postsynaptic dopamine D2 receptors. Current opinion in pharmacology, 2009. 9(1): p. 53-58.
74. Simpson, E.H., C. Kellendonk, and E. Kandel, A possible role for the striatum in the pathogenesis of the cognitive symptoms of schizophrenia. Neuron, 2010. 65(5): p. 585-596.
75. Lesting, J., J. Neddens, and G. Teuchert-Noodt, Ontogeny of the dopamine innervation in the nucleus accumbens of gerbils. Brain research, 2005. 1066(1-2): p. 16-23.
76. Sanford, N. and T.S. Woodward, Functional Delineation of Prefrontal Networks Underlying Working Memory in Schizophrenia: A Cross-data-set Examination. Journal of Cognitive Neuroscience, 2021. 33(9): p. 1880-1908.
77. Meador-Woodruff, J.H., et al., Dopamine receptor transcript expression in striatum and prefrontal and occipital cortex: focal abnormalities in orbitofrontal cortex in schizophrenia. Archives of general psychiatry, 1997. 54(12): p. 1089-1095.
78. Kwak, Y.T., et al., Change of dopamine receptor mRNA expression in lymphocyte of schizophrenic patients. BMC medical genetics, 2001. 2(1): p. 1-9.
79. Albert, K.A., et al., Evidence for decreased DARPP-32 in the prefrontal cortex of patients with schizophrenia. Archives of general psychiatry, 2002. 59(8): p. 705-712.
80. Berridge, M.J., Inositol trisphosphate and calcium signalling mechanisms. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 2009. 1793(6): p. 933-940.
81. Berridge, M.J., The inositol trisphosphate/calcium signaling pathway in health and disease. Physiological reviews, 2016. 96(4): p. 1261-1296.
82. O’Brien, W.T., et al., Glycogen synthase kinase-3 is essential for β-arrestin-2 complex formation and lithium-sensitive behaviors in mice. The Journal of clinical investigation, 2011. 121(9).
83. Koros, E. and C. Dorner-Ciossek, The role of glycogen synthase kinase-3beta in schizophrenia. Drug news & perspectives, 2007. 20(7): p. 437-445.
84. Beasley, C., et al., Glycogen synthase kinase-3β immunoreactivity is reduced in the prefrontal cortex in schizophrenia. Neuroscience Letters, 2001. 302(2-3): p. 117-120.
85. Emamian, E.S., et al., Convergent evidence for impaired AKT1-GSK3beta signaling in schizophrenia. Nat Genet, 2004. 36(2): p. 131-7.
86. Weickert, C.S., et al., Human dysbindin (dtnbp1) gene expression innormal brain and in schizophrenic prefrontal cortex and midbrain. Archives of general psychiatry, 2004. 61(6): p. 544-555.
87. Iizuka, Y., et al., Evidence that the BLOC-1 protein dysbindin modulates dopamine D2 receptor internalization and signaling but not D1 internalization. Journal of Neuroscience, 2007. 27(45): p. 12390-12395.
88. Scheggia, D., et al., Variations in Dysbindin-1 are associated with cognitive response to antipsychotic drug treatment. Nat Commun, 2018. 9(1): p. 2265.
89. Scheggia, D., et al., Variations in Dysbindin-1 are associated with cognitive response to antipsychotic drug treatment. Nature communications, 2018. 9(1): p. 1-11.
90. Stahl, S.M., Mechanism of action of brexpiprazole: comparison with aripiprazole. CNS Spectr, 2016. 21(1): p. 1-6.
91. Yoshimi, N., T. Futamura, and K. Hashimoto, Improvement of dizocilpine-induced social recognition deficits in mice by brexpiprazole, a novel serotonin–dopamine activity modulator. European Neuropsychopharmacology, 2015. 25(3): p. 356-364.
92. Bessieres, B., O. Nicole, and B. Bontempi, Assessing recent and remote associative olfactory memory in rats using the social transmission of food preference paradigm. Nature Protocols, 2017. 12(7): p. 1415-1436.
93. Loureiro, M., et al., Social transmission of food safety depends on synaptic plasticity in the prefrontal cortex. Science, 2019. 364(6444): p. 991-995.
94. Vazdarjanova, A., et al., Spatial exploration induces ARC, a plasticity‐related immediate‐early gene, only in calcium/calmodulin‐dependent protein kinase II‐positive principal excitatory and inhibitory neurons of the rat forebrain. Journal of Comparative Neurology, 2006. 498(3): p. 317-329.
95. Harda, Z., et al., Autophosphorylation of αCaMKII affects social interactions in mice. Genes, Brain and Behavior, 2018. 17(5): p. e12457.
96. Williamson, C.M., et al., Social hierarchy position in female mice is associated with plasma corticosterone levels and hypothalamic gene expression. Scientific Reports, 2019. 9(1): p. 1-14.
97. Eisenegger, C., J. Haushofer, and E. Fehr, The role of testosterone in social interaction. Trends in cognitive sciences, 2011. 15(6): p. 263-271.
98. Duque-Wilckens, N. and B.C. Trainor, Behavioral neuroendocrinology of female aggression, in Oxford research encyclopedia of neuroscience. 2017.
99. Wu, M.V., et al., Estrogen masculinizes neural pathways and sex-specific behaviors. Cell, 2009. 139(1): p. 61-72.
100. Mehta, P.H., et al., Hormonal underpinnings of status conflict: Testosterone and cortisol are related to decisions and satisfaction in the hawk-dove game. Hormones and Behavior, 2017. 92: p. 141-154.
101. Creel, S., Social dominance and stress hormones. Trends in ecology & evolution, 2001. 16(9): p. 491-497.
102. Creel, S., Dominance, aggression, and glucocorticoid levels in social carnivores. Journal of Mammalogy, 2005. 86(2): p. 255-264.
103. Florido, A., et al., Sex differences in fear memory consolidation via Tac2 signaling in mice. Nature communications, 2021. 12(1): p. 1-19.
104. Ferretti, V., et al., Oxytocin signaling in the central amygdala modulates emotion discrimination in mice. Current Biology, 2019. 29(12): p. 1938-1953. e6.
105. Guastella, A.J., P.B. Mitchell, and F. Mathews, Oxytocin enhances the encoding of positive social memories in humans. Biological psychiatry, 2008. 64(3): p. 256-258.
106. Skuse, D.H., et al., Common polymorphism in the oxytocin receptor gene (OXTR) is associated with human social recognition skills. Proceedings of the National Academy of Sciences, 2014. 111(5): p. 1987-1992.
107. Pobbe, R.L., et al., Oxytocin receptor knockout mice display deficits in the expression of autism-related behaviors. Hormones and behavior, 2012. 61(3): p. 436-444.
108. Becker, J.B. and E. Chartoff, Sex differences in neural mechanisms mediating reward and addiction. Neuropsychopharmacology, 2019. 44(1): p. 166-183.
109. Zachry, J.E., et al., Sex differences in dopamine release regulation in the striatum. Neuropsychopharmacology, 2021. 46(3): p. 491-499.
110. Williams, O.O., et al., Sex Differences in Dopamine Receptors and Relevance to Neuropsychiatric Disorders. Brain Sciences, 2021. 11(9): p. 1199.
111. Andersen, S.L., et al., Sex differences in dopamine receptor overproduction and elimination. Neuroreport, 1997. 8(6): p. 1495-1497.
112. Hasbi, A., et al., Sex difference in dopamine D1-D2 receptor complex expression and signaling affects depression-and anxiety-like behaviors. Biology of sex differences, 2020. 11(1): p. 1-17.
113. Orendain-Jaime, E.N., J.M. Ortega-Ibarra, and S.J. López-Pérez, Evidence of sexual dimorphism in D1 and D2 dopaminergic receptors expression in frontal cortex and striatum of young rats. Neurochemistry International, 2016. 100: p. 62-66.
114. Weinstein, J.J., et al., Pathway-specific dopamine abnormalities in schizophrenia. Biological psychiatry, 2017. 81(1): p. 31-42.
115. Ripke, S., et al., Biological insights from 108 schizophrenia-associated genetic loci. Nature, 2014. 511(7510): p. 421-+.
116. Huentelman, M.J., et al., Association of SNPs in EGR3 and ARC with schizophrenia supports a biological pathway for schizophrenia risk. PloS one, 2015. 10(10): p. e0135076.
117. Fromer, M., et al., De novo mutations in schizophrenia implicate synaptic networks. Nature, 2014. 506(7487): p. 179-184.
118. Purcell, S.M., et al., A polygenic burden of rare disruptive mutations in schizophrenia. Nature, 2014. 506(7487): p. 185-190.
119. Guillozet-Bongaarts, A., et al., Altered gene expression in the dorsolateral prefrontal cortex of individuals with schizophrenia. Molecular psychiatry, 2014. 19(4): p. 478-485.
120. Ji, Y., et al., Role of dysbindin in dopamine receptor trafficking and cortical GABA function. Proceedings of the National Academy of Sciences, 2009. 106(46): p. 19593-19598.
121. Binjumah, M., J. Ajarem, and M. Ahmad, Effects of the perinatal exposure of Gum Arabic on the development, behavior and biochemical parameters of mice offspring. Saudi Journal of Biological Sciences, 2018. 25(7): p. 1332-1338.

指導教授

黃佳瑜(Chia-Yu Huang)

審核日期

2022-7-25

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