請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/46143完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 賴文崧(Wen-Sung Lai) | |
| dc.contributor.author | Yi-Wen Chen | en |
| dc.contributor.author | 陳怡文 | zh_TW |
| dc.date.accessioned | 2021-06-15T04:55:25Z | - |
| dc.date.available | 2015-08-02 | |
| dc.date.copyright | 2010-08-02 | |
| dc.date.issued | 2010 | |
| dc.date.submitted | 2010-07-29 | |
| dc.identifier.citation | Chapter 1
Abi-Dargham, A., Mawlawi, O., Lombardo, I., Gil, R., Martinez, D., Huang, Y., et al. (2002). Prefrontal dopamine D1 receptors and working memory in schizophrenia. Journal of Neuroscience, 22, 3708-3719. Aleman, A., Kahn, R. S., & Selten, J.-P. (2003). Sex differences in the risk of schizophrenia: evidence from meta-analysis. Archives of General Psychiatry, 60, 565-571. Alessi, D. R., Andjelkovic, M., Caudwell, B., Cron, P., Morrice, N., Cohen, P., et al. (1996). Mechanism of activation of protein kinase B by insulin and IGF-1. EMBO Journal, 15, 6541-6551. Arguello, P. A., & Gogos, J. A. (2006). Modeling Madness in Mice: One Piece at a Time. Neuron, 52, 179-196. Bajestan, S. N., Sabouri, A. H., Nakamura, M., Takashima, H., Keikhaee, M. R., Behdani, F., et al. (2006). Association of AKT1 haplotype with the risk of schizophrenia in Iranian population. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 141B, 383-386. Baumeister, A. A., & Francis, J. L. (2002). Historical development of the dopamine hypothesis of schizophrenia. Journal of the History of the Neurosciences, 11, 265-277. Beaulieu, J.-M., Sotnikova, T. D., Yao, W.-D., Kockeritz, L., Woodgett, J. R., Gainetdinov, R. R., et al. (2004). Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade. Proceedings of the National Academy of Sciences of the United States of America, 101, 5099-5104. Beaulieu, J.-M., Sotnikova, T. D., Marion, S., Lefkowitz, R. J., Gainetdinov, R. R., & Caron, M. G. (2005). An Akt/beta-arrestin 2/PP2A signaling complex mediates dopaminergic neurotransmission and behavior. Cell, 122, 261-273. Beaulieu, J.-M., Tirotta, E., Sotnikova, T. D., Masri, B., Salahpour, A., Gainetdinov, R. R., et al. (2007). Regulation of Akt Signaling by D2 and D3 Dopamine Receptors In Vivo. Journal of Neuroscience, 27, 881-885. Beaulieu, J.-M., Gainetdinov, R. R., & Caron, M. G. (2009). Akt/GSK3 Signaling in the Action of Psychotropic Drugs. Annual Review of Pharmacology and Toxicology, 49, 327-347. Brazil, D. P., & Hemmings, B. A. (2001). Ten years of protein kinase B signalling: a hard Akt to follow. Trends in Biochemical Sciences, 26, 657-664. Cannon, M., Jones, P. B., & Murray, R. M. (2002). Obstetric complications and schizophrenia: historical and meta-analytic review. American Journal of Psychiatry, 159, 1080-1092. Canuso, C. M., Goldstein, J. M., & Green, A. I. (1998). The evaluation of women with schizophrenia. Psychopharmacology Bulletin, 34, 271-277. Cardona-Gomez, P., Perez, M., Avila, J., Garcia-Segura, L. M., & Wandosell, F. (2004). Estradiol inhibits GSK3 and regulates interaction of estrogen receptors, GSK3, and beta-catenin in the hippocampus. Molecular and Cellular Neuroscience, 25, 363-373. Castle, D. J., Wessely, S., & Murray, R. M. (1993). Sex and schizophrenia: effects of diagnostic stringency, and associations with and premorbid variables. British Journal of Psychiatry, 162, 658-664. Catts, V. S., & Catts, S. V. (2000). Apoptosis and schizophrenia: is the tumour suppressor gene, p53, a candidate susceptibility gene? Schizophrenia Research, 41, 405-415. Chalecka-Franaszek, E., & Chuang, D. M. (1999). Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons. Proceedings of the National Academy of Sciences of the United States of America, 96, 8745-8750. Cho, H., Thorvaldsen, J. L., Chu, Q., Feng, F., & Birnbaum, M. J. (2001). Akt1/PKBalpha is required for normal growth but dispensable for maintenance of glucose homeostasis in mice. Journal of Biological Chemistry, 276, 38349-38352. Cohen, M., Dembling, B., & Schorling, J. (2002). The association between schizophrenia and cancer: a population-based mortality study. Schizophrenia Research, 57, 139-146. Cowell, P. E., Kostianovsky, D. J., Gur, R. C., Turetsky, B. I., & Gur, R. E. (1996). Sex differences in neuroanatomical and clinical correlations in schizophrenia. American Journal of Psychiatry, 153, 799-805. Coyle, J. T. (2006). Glutamate and schizophrenia: beyond the dopamine hypothesis. Cellular and Molecular Neurobiology, 26, 365-384. Crabbe, J. C., Wahlsten, D., & Dudek, B. C. (1999). Genetics of mouse behavior: interactions with laboratory environment. Science, 284, 1670-1672. Downward, J. (1998). Mechanisms and consequences of activation of protein kinase B/Akt. Current Opinion in Cell Biology, 10, 262-267. Elsworth, J. D., & Roth, R. H. (1997). Dopamine synthesis, uptake, metabolism, and receptors: relevance to gene therapy of Parkinson's disease. Experimental Neurology, 144, 4-9. Emamian, E. S., Hall, D., Birnbaum, M. J., Karayiorgou, M., & Gogos, J. A. (2004). Convergent evidence for impaired AKT1-GSK3β signaling in schizophrenia. Nature Genetics, 36, 131-137. Fayard, E., Tintignac, L. A., Baudry, A., & Hemmings, B. A. (2005). Protein kinase B/Akt at a glance. Journal of Cell Science, 118, 5675-5678. Franke, T. F. (2008). PI3K/Akt: getting it right matters. Oncogene, 27, 6473-6488. Galetic, I., Maira, S. M., Andjelkovic, M., & Hemmings, B. A. (2003). Negative regulation of ERK and Elk by protein kinase B modulates c-Fos transcription. Journal of Biological Chemistry, 278, 4416-4423. Gervais, M., Dugourd, C., Muller, L., Ardidie, C., Canton, B., Loviconi, L., et al. (2006). Akt down-regulates ERK1/2 nuclear localization and angiotensin II-induced cell proliferation through PEA-15. Molecular Biology of the Cell, 17, 3940-3951. Gogos, J. A., & Gerber, D. (2006). Schizophrenia susceptibility genes: emergence of positional candidates and future directions. Trends in Pharmacological Sciences, 27, 226-233. Goldman-Rakic, P. S., Muly, E. C., 3rd, & Williams, G. V. (2000). D(1) receptors in prefrontal cells and circuits. Brain Research. Brain Research Reviews, 31, 295-301. Gottesman, II, & Gould, T. D. (2003). The endophenotype concept in psychiatry: etymology and strategic intentions. American Journal of Psychiatry, 160, 636-645. Greengard, P. (2001). The Neurobiology of Slow Synaptic Transmission. Science, 294, 1024-1030. Hafner, H., Riecher, A., Maurer, K., Loffler, W., Munk-Jorgensen, P., & Stromgren, E. (1989). How does gender influence age at first hospitalization for schizophrenia? A transnational case register study. Psychological Medicine, 19, 903-918. Hafner, H., an der Heiden, W., Behrens, S., Gattaz, W. F., Hambrecht, M., Loffler, W., et al. (1998). Causes and Consequences of the Gender Difference in Age at Onset of Schizophrenia. Schizophrenia Bulletin, 24, 99-113. Heresco-Levy, U., Ermilov, M., Shimoni, J., Shapira, B., Silipo, G., & Javitt, D. C. (2002). Placebo-controlled trial of D-cycloserine added to conventional neuroleptics, olanzapine, or risperidone in schizophrenia. American Journal of Psychiatry, 159, 480-482. Ikeda, M., Iwata, N., Suzuki, T., Kitajima, T., Yamanouchi, Y., Kinoshita, Y., et al. (2004). Association of AKT1 with schizophrenia confirmed in a Japanese population. Biological Psychiatry, 56, 698-700. Ikeda, M., Iwata, N., Suzuki, T., Kitajima, T., Yamanouchi, Y., Kinoshita, Y., et al. (2006). Positive association of AKT1 haplotype to Japanese methamphetamine use disorder. International Journal of Neuropsychopharmacology, 9, 77-81. Ivanova, T., Mendez, P., Garcia-Segura, L. M., & Beyer, C. (2002). Rapid stimulation of the PI3-kinase/Akt signalling pathway in developing midbrain neurones by oestrogen. Journal of Neuroendocrinology, 14, 73-79. Jablensky, A. V., Morgan, V., Zubrick, S. R., Bower, C., & Yellachich, L. A. (2005). Pregnancy, delivery, and neonatal complications in a population cohort of women with schizophrenia and major affective disorders. American Journal of Psychiatry, 162, 79-91. Javitt, D. C. (2007). Glutamate and schizophrenia: phencyclidine, N-methyl-D-aspartate receptors, and dopamine-glutamate interactions. International Review Neurobiology, 78, 69-108. Jaworski, J., Spangler, S., Seeburg, D. P., Hoogenraad, C. C., & Sheng, M. (2005). Control of dendritic arborization by the phosphoinositide-3'-kinase-Akt-mammalian target of rapamycin pathway. Journal of Neuroscience, 25, 11300-11312. Kalivas, P. W., & Stewart, J. (1991). Dopamine transmission in the initiation and expression of drug- and stress-induced sensitization of motor activity. Brain Research. Brain Research Reviews, 16, 223-244. Kalkman, H. O. (2006). The role of the phosphatidylinositide 3-kinase-protein kinase B pathway in schizophrenia. Pharmacology and Therapeutics, 110, 117-134. Kapur, S., & Remington, G. (2001). Atypical antipsychotics: new directions and new challenges in the treatment of schizophrenia. Annual Review of Medicine, 52, 503-517. Kapur, S., & Mamo, D. (2003). Half a century of antipsychotics and still a central role for dopamine D2 receptors. Progress in Neuropsychopharmacology and Biological Psychiatry, 27, 1081-1090. Kellendonk, C., Simpson, E. H., & Kandel, E. R. (2009). Modeling cognitive endophenotypes of schizophrenia in mice. Trends in Neurosciences, 32, 347-358. Kokkinidis, L., & Anisman, H. (1981). Amphetamine psychosis and schizophrenia: a dual model. Neuroscience and Biobehavioral Reviews, 5, 449-461. Kunugi, H., Nanko, S., & Murray, R. M. (2001). Obstetric complications and schizophrenia: prenatal underdevelopment and subsequent neurodevelopmental impairment. Britsh Jouranl of Psychiatry. Supplement, 40, s25-29. Kwon, C. H., Luikart, B. W., Powell, C. M., Zhou, J., Matheny, S. A., Zhang, W., et al. (2006). Pten regulates neuronal arborization and social interaction in mice. Neuron, 50, 377-388. Lai, W.-S., Xu, B., Westphal, K. G. C., Paterlini, M., Olivier, B., Pavlidis, P., et al. (2006). Akt1 deficiency affects neuronal morphology and predisposes to abnormalities in prefrontal cortex functioning. Proceedings of the National Academy of Sciences of the United States of America, 103, 16906-16911. Lane, H. Y., Chang, Y. C., Liu, Y. C., Chiu, C. C., & Tsai, G. E. (2005). Sarcosine or D-serine add-on treatment for acute exacerbation of schizophrenia: a randomized, double-blind, placebo-controlled study. Archives of General Psychiatry, 62, 1196-1204. Lee, K., Joo, E., Jeong, S., Kang, U., Roh, M., Kim, S., et al. (2009). No association between AKT1 polymorphism and schizophrenia: A case-control study in a Korean population and a meta-analysis. Neuroscience Research, 66, 238-245. Lewis, C. M., Levinson, D. F., Wise, L. H., DeLisi, L. E., Straub, R. E., Hovatta, I., et al. (2003). Genome scan meta-analysis of schizophrenia and bipolar disorder, part II: Schizophrenia. American Journal of Human Genetics, 73, 34-48. Lewis, D. A., & Lieberman, J. A. (2000). Catching up on schizophrenia: natural history and neurobiology. Neuron, 28, 325-334. Lewis, D. A., Hashimoto, T., & Volk, D. W. (2005). Cortical inhibitory neurons and schizophrenia. Nature Reviews. Neuroscience, 6, 312-324. Lewis, D. A., & Sweet, R. A. (2009). Schizophrenia from a neural circuitry perspective: advancing toward rational pharmacological therapies. Journal of Clinical Investigation, 119, 706-716. Li, B., Woo, R. S., Mei, L., & Malinow, R. (2007). The neuregulin-1 receptor erbB4 controls glutamatergic synapse maturation and plasticity. Neuron, 54, 583-597. Lichtermann, D., Ekelund, J., Pukkala, E., Tanskanen, A., & Lonnqvist, J. (2001). Incidence of cancer among persons with schizophrenia and their relatives. Archives of General Psychiatry, 58, 573-578. Lindamer, L. A., Lohr, J. B., Harris, M. J., & Jeste, D. V. (1997). Gender, estrogen, and schizophrenia. Psychopharmacology Bulletin, 33, 221-228. Liu, Y., Tao, Y. M., Woo, R. S., Xiong, W. C., & Mei, L. (2007). Stimulated ErbB4 internalization is necessary for neuregulin signaling in neurons. Biochemical and Biophysical Research Communications, 354, 505-510. Liu, Y.-L., Fann, C. S.-J., Liu, C.-M., Wu, J.-Y., Hung, S.-I., Chan, H.-Y., et al. (2006). Absence of significant associations between four AKT1 SNP markers and schizophrenia in the Taiwanese population. Psychiatric Genetics, 16, 39-41. Mathur, A., Law, M. H., Megson, I. L., Shaw, D. J., & Wei, J. (2010). Genetic association of the AKT1 gene with schizophrenia in a British population. Psychiatric Genetics, 20, 118-122. McEvoy, J. P., Lieberman, J. A., Stroup, T. S., Davis, S. M., Meltzer, H. Y., Rosenheck, R. A., et al. (2006). Effectiveness of clozapine versus olanzapine, quetiapine, and risperidone in patients with chronic schizophrenia who did not respond to prior atypical antipsychotic treatment. American Journal of Psychiatry, 163, 600-610. McGrath, J. J. (2006). Variations in the incidence of schizophrenia: data versus dogma. Schizophrenia Bulletin, 32, 195-197. McGrath, J. J., Saha, S., Welham, J., El Saadi, O., MacCauley, C., & Chant, D. (2004). A systematic review of the incidence of schizophrenia: the distribution of rates and the influence of sex, urbanicity, migrant status and methodology. BMC medicine, 2, 13. Mendez, P., Wandosell, F., & Garcia-Segura, L. M. (2006). Cross-talk between estrogen receptors and insulin-like growth factor-I receptor in the brain: cellular and molecular mechanisms. Frontiers in Neuroendocrinology, 27, 391-403. Milner, J. D., & Wurtman, R. J. (1986). Catecholamine synthesis: physiological coupling to precursor supply. Biochemical Pharmacology, 35, 875-881. Missale, C., Nash, S. R., Robinson, S. W., Jaber, M., & Caron, M. G. (1998). Dopamine receptors: from structure to function. Physiological Reviews, 78, 189-225. Norton, N., Williams, H. J., & Owen, M. J. (2006). An update on the genetics of schizophrenia. Current Opinion in Psychiatry, 19, 158-164. Norton, N., Williams, H., Dwyer, S., Carroll, L., Peirce, T., Moskvina, V., et al. (2007). Association analysis of AKT1 and schizophrenia in a UK case control sample. Schizophrenia Research, 93, 58-65. Ohtsuki, T., Inada, T., & Arinami, T. (2004). Failure to confirm association between AKT1 haplotype and schizophrenia in a Japanese case-control population. Molecular Psychiatry, 9, 981-983. Persad, S., Attwell, S., Gray, V., Mawji, N., Deng, J. T., Leung, D., et al. (2001). Regulation of protein kinase B/Akt-serine 473 phosphorylation by integrin-linked kinase: critical roles for kinase activity and amino acids arginine 211 and serine 343. Journal of Biological Chemistry, 276, 27462-27469. Post, R. M., Weiss, S. R., Fontana, D., & Pert, A. (1992). Conditioned sensitization to the psychomotor stimulant cocaine. Annals of the New York Academy of Sciences, 654, 386-399. Powell, C. M., & Miyakawa, T. (2006). Schizophrenia-relevant behavioral testing in rodent models: a uniquely human disorder? Biological Psychiatry, 59, 1198-1207. Qin, Y., Zhu, Y., Baumgart, J. P., Stornetta, R. L., Seidenman, K., Mack, V., et al. (2005). State-dependent Ras signaling and AMPA receptor trafficking. Genes and Development, 19, 2000-2015. Ragland, J. D., Yoon, J., Minzenberg, M. J., & Carter, C. S. (2007). Neuroimaging of cognitive disability in schizophrenia: search for a pathophysiological mechanism. International Review of Psychiatry, 19, 417-427. Riley, B., & Kendler, K. S. (2006). Molecular genetic studies of schizophrenia. European Journal of Human Genetics, 14, 669-680. Robinson, T. E., & Becker, J. B. (1986). Enduring changes in brain and behavior produced by chronic amphetamine administration: a review and evaluation of animal models of amphetamine psychosis. Brain Research, 396, 157-198. Robinson, T. E., & Berridge, K. C. (1993). The neural basis of drug craving: an incentive-sensitization theory of addiction. Brain Research. Brain Research Reviews, 18, 247-291. Rosenzweig, M. R., Breedlove, S. M., & Watson, N. V. (2005). Biological psychology: an introduction to behavioral and cognitive neuroscience (4th ed.). Sunderland: Sinauer Associates, Inc. Sale, E. M., & Sale, G. J. (2008). Protein kinase B: signalling roles and therapeutic targeting. Cellular and Molecular Life Science, 65, 113-127. Scheid, M. P., & Woodgett, J. R. (2001). PKB/AKT: functional insights from genetic models. Nature Reviews. Molecular Cell Biology, 2, 760-768. Schwab, S. G., Hoefgen, B., Hanses, C., Hassenbach, M. B., Albus, M., Lerer, B., et al. (2005). Further evidence for association of variants in the AKT1 gene with schizophrenia in a sample of European sib-pair families. Biological Psychiatry, 58, 446-450. Schwab, S. G., & Wildenauer, D. B. (2009). Update on key previously proposed candidate genes for schizophrenia. Current Opinion in Psychiatry, 22, 147-153. Seeman, M. V. (1983). Interaction of sex, age, and neuroleptic dose. Comprehensive Psychiatry, 24, 125-128. Seeman, M. V. (1997). The 'marriage bed': brain and outcome in schizophrenia. Canadian Journal of Psychiatry, 42, 19-20. Segal, D. S., & Kuczenski, R. (1997). Repeated binge exposures to amphetamine and methamphetamine: behavioral and neurochemical characterization. Journal of Pharmacology and Experimental Therapeutics, 282, 561-573. Simpson, E. H., Kellendonk, C., & Kandel, E. (2010). A possible role for the striatum in the pathogenesis of the cognitive symptoms of schizophrenia. Neuron, 65, 585-596. Snyder, K. (2006). Kurt Snyder's personal experience with schizophrenia. Schizophrenia Bulletin, 32, 209-211. Strange, P. G. (2001). Antipsychotic drugs: importance of dopamine receptors for mechanisms of therapeutic actions and side effects. Pharmacological Reviews, 53, 119-133. Sullivan, P. F., Kendler, K. S., & Neale, M. C. (2003). Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies. Archives of General Psychiatry, 60, 1187-1192. Swerdlow, N. R., Vaccarino, F. J., Amalric, M., & Koob, G. F. (1986). The neural substrates for the motor-activating properties of psychostimulants: a review of recent findings. Pharmacology, Biochemistry and Behavior, 25, 233-248. Tessner, K. D., Mittal, V., & Walker, E. F. (2009). Longitudinal Study of Stressful Life Events and Daily Stressors Among Adolescents at High Risk for Psychotic Disorders. Schizophrenia Bulletin, doi:10.1093/schbul/sbp087. Thiselton, D. L., Vladimirov, V. I., Kuo, P.-H., McClay, J., Wormley, B., Fanous, A., et al. (2008). AKT1 is associated with schizophrenia across multiple symptom dimensions in the Irish study of high density schizophrenia families. Biological Psychiatry, 63, 449-457. Tsai, L.-H., & Gleeson, J. G. (2005). Nucleokinesis in neuronal migration. Neuron, 46, 383-388. Vezina, P. (1996). D1 dopamine receptor activation is necessary for the induction of sensitization by amphetamine in the ventral tegmental area. Journal of Neuroscience, 16, 2411-2420. Wang, Q., Liu, L., Pei, L., Ju, W., Ahmadian, G., Lu, J., et al. (2003). Control of synaptic strength, a novel function of Akt. Neuron, 38, 915-928. Woo, R. S., Li, X. M., Tao, Y., Carpenter-Hyland, E., Huang, Y. Z., Weber, J., et al. (2007). Neuregulin-1 enhances depolarization-induced GABA release. Neuron, 54, 599-610. Xu, M.-Q., Xing, Q.-H., Zheng, Y.-L., Li, S., Gao, J.-J., He, G., et al. (2007). Association of AKT1 gene polymorphisms with risk of schizophrenia and with response to antipsychotics in the Chinese population. The Journal of Clinical Psychiatry, 68, 1358-1367. Chapter 2 Aleman, A., Kahn, R. S., & Selten, J.-P. (2003). Sex differences in the risk of schizophrenia: evidence from meta-analysis. Archives of General Psychiatry, 60, 565-571. Bajestan, S. N., Sabouri, A. H., Nakamura, M., Takashima, H., Keikhaee, M. R., Behdani, F., et al. (2006). Association of AKT1 haplotype with the risk of schizophrenia in Iranian population. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 141B, 383-386. Beaulieu, J.-M., Sotnikova, T. D., Yao, W.-D., Kockeritz, L., Woodgett, J. R., Gainetdinov, R. R., et al. (2004). Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade. Proceedings of the National Academy of Sciences of the United States of America, 101, 5099-5104. Beaulieu, J.-M., Sotnikova, T. D., Marion, S., Lefkowitz, R. J., Gainetdinov, R. R., & Caron, M. G. (2005). An Akt/beta-arrestin 2/PP2A signaling complex mediates dopaminergic neurotransmission and behavior. Cell, 122, 261-273. Beaulieu, J.-M., Gainetdinov, R. R., & Caron, M. G. (2007). The Akt-GSK-3 signaling cascade in the actions of dopamine. Trends in Pharmacological Sciences, 28, 166-172. Beaulieu, J.-M., Gainetdinov, R. R., & Caron, M. G. (2009). Akt/GSK3 Signaling in the Action of Psychotropic Drugs. Annual Review of Pharmacology and Toxicology, 49, 327-347. Braff, D. L., Light, G. A., Ellwanger, J., Sprock, J., & Swerdlow, N. R. (2005). Female schizophrenia patients have prepulse inhibition deficits. Biological Psychiatry, 57, 817-820. Brody, S. A., Conquet, F., & Geyer, M. A. (2004). Effect of antipsychotic treatment on the prepulse inhibition deficit of mGluR5 knockout mice. Psychopharmacology, 172, 187-195. Campbell, L. E., Hughes, M., Budd, T. W., Cooper, G., Fulham, W. R., Karayanidis, F., et al. (2007). Primary and secondary neural networks of auditory prepulse inhibition: a functional magnetic resonance imaging study of sensorimotor gating of the human acoustic startle response. European Journal of Neuroscience, 26, 2327-2333. Chalecka-Franaszek, E., & Chuang, D. M. (1999). Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons. Proceedings of the National Academy of Sciences of the United States of America, 96, 8745-8750. Cho, H., Thorvaldsen, J. L., Chu, Q., Feng, F., & Birnbaum, M. J. (2001). Akt1/PKBalpha is required for normal growth but dispensable for maintenance of glucose homeostasis in mice. Journal of Biological Chemistry, 276, 38349-38352. Cross, D. A., Culbert, A. A., Chalmers, K. A., Facci, L., Skaper, S. D., & Reith, A. D. (2001). Selective small-molecule inhibitors of glycogen synthase kinase-3 activity protect primary neurones from death. Journal of Neurochemistry, 77, 94-102. Dorph-Petersen, K.-A., Delevich, K. M., Marcsisin, M. J., Zhang, W., Sampson, A. R., Gundersen, H. J. G., et al. (2009). Pyramidal neuron number in layer 3 of primary auditory cortex of subjects with schizophrenia. Brain Research, 1285, 42-57. Downward, J. (1998). Mechanisms and consequences of activation of protein kinase B/Akt. Current Opinion in Cell Biology, 10, 262-267. Dulawa, S. C., Gross, C., Stark, K. L., Hen, R., & Geyer, M. A. (2000). Knockout mice reveal opposite roles for serotonin 1A and 1B receptors in prepulse inhibition. Neuropsychopharmacology, 22, 650-659. Duncan, G. E., Moy, S. S., Lieberman, J. A., & Koller, B. H. (2006). Effects of haloperidol, clozapine, and quetiapine on sensorimotor gating in a genetic model of reduced NMDA receptor function. Psychopharmacology, 184, 190-200. Emamian, E. S., Hall, D., Birnbaum, M. J., Karayiorgou, M., & Gogos, J. A. (2004). Convergent evidence for impaired AKT1-GSK3β signaling in schizophrenia. Nature Genetics, 36, 131-137. Feng, G., Mellor, R. H., Bernstein, M., Keller-Peck, C., Nguyen, Q. T., Wallace, M., et al. (2000). Imaging neuronal subsets in transgenic mice expressing multiple spectral variants of GFP. Neuron, 28, 41-51. Gavrilescu, M., Rossell, S., Stuart, G. W., Shea, T. L., Innes-Brown, H., Henshall, K., et al. (2009). Reduced connectivity of the auditory cortex in patients with auditory hallucinations: a resting state functional magnetic resonance imaging study. Psychological Medicine, 40,1149-1158. Gogos, A., Bogeski, M., & van den Buuse, M. (2008). Role of serotonin-1A receptors in the action of antipsychotic drugs: comparison of prepulse inhibition studies in mice and rats and relevance for human pharmacology. Behavioural Pharmacology, 19, 548-561. Grigoriadis, S., & Seeman, M. V. (2002). The Role of Estrogen in Schizophrenia: Implications for Schizophrenia Practice Guidelines for Women. [Article]. Canadian Journal of Psychiatry, 47, 437. Hafner, H., an der Heiden, W., Behrens, S., Gattaz, W. F., Hambrecht, M., Loffler, W., et al. (1998). Causes and Consequences of the Gender Difference in Age at Onset of Schizophrenia. Schizophrenia Bulletin, 24, 99-113. Hubl, D., Koenig, T., Strik, W. K., Garcia, L. M., & Dierks, T. (2007). Competition for neuronal resources: how hallucinations make themselves heard. British Journal of Psychiatry, 190, 57-62. Ikeda, M., Iwata, N., Suzuki, T., Kitajima, T., Yamanouchi, Y., Kinoshita, Y., et al. (2004). Association of AKT1 with schizophrenia confirmed in a Japanese population. Biological Psychiatry, 56, 698-700. Ikeda, M., Iwata, N., Suzuki, T., Kitajima, T., Yamanouchi, Y., Kinoshita, Y., et al. (2006). Positive association of AKT1 haplotype to Japanese methamphetamine use disorder. International Journal of Neuropsychopharmacology, 9, 77-81. Ikeda, M., Yamanouchi, Y., Kinoshita, Y., Kitajima, T., Yoshimura, R., Hashimoto, S., et al. (2008). Variants of dopamine and serotonin candidate genes as predictors of response to risperidone treatment in first-episode schizophrenia. Pharmacogenomics, 9, 1437-1443. Karege, F., Perroud, N., Schurhoff, F., Meary, A., Marillier, G., Burkhardt, S., et al. (2010). Association of AKT1 gene variants and protein expression in both schizophrenia and bipolar disorder. Genes, Brain, and Behavior, doi:10.1111/j.1601-183X.2010.00578.x. Kim, J. Y., Duan, X., Liu, C. Y., Jang, M.-H., Guo, J. U., Pow-anpongkul, N., et al. (2009). DISC1 regulates new neuron development in the adult brain via modulation of AKT-mTOR signaling through KIAA1212. Neuron, 63, 761-773. Lai, W.-S., Xu, B., Westphal, K. G. C., Paterlini, M., Olivier, B., Pavlidis, P., et al. (2006). Akt1 deficiency affects neuronal morphology and predisposes to abnormalities in prefrontal cortex functioning. Proceedings of the National Academy of Sciences of the United States of America, 103, 16906-16911. Lee, K., Joo, E., Jeong, S., Kang, U., Roh, M., Kim, S., et al. (2009). No association between AKT1 polymorphism and schizophrenia: A case-control study in a Korean population and a meta-analysis. Neuroscience Research, 66, 238-245. Li, X., Zhu, W., Roh, M.-S., Friedman, A. B., Rosborough, K., & Jope, R. S. (2004). In vivo regulation of glycogen synthase kinase-3beta (GSK3beta) by serotonergic activity in mouse brain. Neuropsychopharmacology, 29, 1426-1431. Liu, Y.-L., Fann, C. S.-J., Liu, C.-M., Wu, J.-Y., Hung, S.-I., Chan, H.-Y., et al. (2006). Absence of significant associations between four AKT1 SNP markers and schizophrenia in the Taiwanese population. Psychiatric Genetics, 16, 39-41. Mao, Y., Ge, X., Frank, C. L., Madison, J. M., Koehler, A. N., Doud, M. K., et al. (2009). Disrupted in schizophrenia 1 regulates neuronal progenitor proliferation via modulation of GSK3beta/beta-catenin signaling. Cell, 136, 1017-1031. McGrath, J. J., Saha, S., Welham, J., El Saadi, O., MacCauley, C., & Chant, D. (2004). A systematic review of the incidence of schizophrenia: the distribution of rates and the influence of sex, urbanicity, migrant status and methodology. BMC Medicine, 2, 13. Meijer, L., Flajolet, M., & Greengard, P. (2004). Pharmacological inhibitors of glycogen synthase kinase 3. Trends in Pharmacological Sciences, 25, 471-480. Miller, J., Tallarida, R., & Unterwald, E. (2009). Cocaine-induced hyperactivity and sensitization are dependent on GSK3. Neuropharmacology, 56, 1116-1123. Norton, N., Williams, H. J., Dwyer, S., Carroll, L., Peirce, T., Moskvina, V., et al. (2007). Association analysis of AKT1 and schizophrenia in a UK case control sample. Schizophrenia Research, 93, 58-65. Ohtsuki, T., Inada, T., & Arinami, T. (2004). Failure to confirm association between AKT1 haplotype and schizophrenia in a Japanese case-control population. Molecular Psychiatry, 9, 981-983. Rabinowicz, E. F., Silipo, G., Goldman, R., & Javitt, D. C. (2000). Auditory sensory dysfunction in schizophrenia: imprecision or distractibility? Archives of General Psychiatry, 57, 1149-1155. Read, D. E., & Gorman, A. M. (2009). Involvement of Akt in neurite outgrowth. Cellular and Molecular Life Sciences, 66, 2975-2984. Salokangas, R. K. R., Honkonen, T., & Saarinen, S. (2003). Women have later onset than men in schizophrenia--but only in its paranoid form. Results of the DSP project. [doi: DOI: 10.1016/j.eurpsy.2003.03.001]. European Psychiatry, 18, 274-281. Scheid, M. P., & Woodgett, J. R. (2001). PKB/AKT: functional insights from genetic models. Nature Reviews. Molecular Cell Biology, 2, 760-768. Schwab, S. G., Hoefgen, B., Hanses, C., Hassenbach, M. B., Albus, M., Lerer, B., et al. (2005). Further evidence for association of variants in the AKT1 gene with schizophrenia in a sample of European sib-pair families. Biological Psychiatry, 58, 446-450. Schwab, S. G., & Wildenauer, D. B. (2009). Update on key previously proposed candidate genes for schizophrenia. Current Opinion in Psychiatry, 22, 147-153. Swerdlow, N. R., Geyer, M. A., & Braff, D. L. (2001). Neural circuit regulation of prepulse inhibition of startle in the rat: current knowledge and future challenges. Psychopharmacology, 156, 194-215. Swerdlow, N. R., Light, G. A., Cadenhead, K. S., Sprock, J., Hsieh, M. H., & Braff, D. L. (2006). Startle gating deficits in a large cohort of patients with schizophrenia: relationship to medications, symptoms, neurocognition, and level of function. Archives of General Psychiatry, 63, 1325-1335. Tan, H.-Y., Nicodemus, K. K., Chen, Q., Li, Z., Brooke, J. K., Honea, R., et al. (2008). Genetic variation in AKT1 is linked to dopamine-associated prefrontal cortical structure and function in humans. Journal of Clinical Investigation, 118, 2200-2208. Thiselton, D. L., Vladimirov, V. I., Kuo, P.-H., McClay, J., Wormley, B., Fanous, A., et al. (2008). AKT1 is associated with schizophrenia across multiple symptom dimensions in the Irish study of high density schizophrenia families. Biological Psychiatry, 63, 449-457. Xu, M.-Q., Xing, Q.-H., Zheng, Y.-L., Li, S., Gao, J.-J., He, G., et al. (2007). Association of AKT1 gene polymorphisms with risk of schizophrenia and with response to antipsychotics in the Chinese population. Journal of Clinical Psychiatry, 68, 1358-1367. Zhao, Z., Ksiezak-Reding, H., Riggio, S., Haroutunian, V., & Pasinetti, G. M. (2006). Insulin receptor deficits in schizophrenia and in cellular and animal models of insulin receptor dysfunction. Schizophrenia Research, 84, 1-14. Chapter 3 Akhondzadeh, S., Nejatisafa, A. A., Amini, H., Mohammadi, M. R., Larijani, B., Kashani, L., et al. (2003). Adjunctive estrogen treatment in women with chronic schizophrenia: a double-blind, randomized, and placebo-controlled trial. Progress in Neuropsychopharmacology and Biological Psychiatry, 27, 1007-1012. Altar, C. A., Hunt, R. A., Jurata, L. W., Webster, M. J., Derby, E., Gallagher, P., et al. (2008). Insulin, IGF-1, and muscarinic agonists modulate schizophrenia-associated genes in human neuroblastoma cells. Biological Psychiatry, 64, 1077-1087. Anderson, L. I., Leipheimer, R. E., & Dluzen, D. E. (2005). Effects of neonatal and prepubertal hormonal manipulations upon estrogen neuroprotection of the nigrostriatal dopaminergic system within female and male mice. Neuroscience, 130, 369-382. Beaulieu, J.-M., Sotnikova, T. D., Yao, W.-D., Kockeritz, L., Woodgett, J. R., Gainetdinov, R. R., et al. (2004). Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade. Proceedings of the National Academy of Sciences of the United States of America, 101, 5099-5104. Beaulieu, J.-M., Sotnikova, T. D., Marion, S., Lefkowitz, R. J., Gainetdinov, R. R., & Caron, M. G. (2005). An Akt/beta-arrestin 2/PP2A signaling complex | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/46143 | - |
| dc.description.abstract | 精神分裂症是一種多因子且嚴重之精神疾患，從人類遺傳學及動物的研究中越來越多的證據顯示Akt1基因可能參與了精神分裂症的致病歷程。相較於以人類為受試所進行的遺傳相關性研究，基因突變小鼠的模式更能直接探究Akt1基因的生物功能以及它在精神分裂症致病性上之因果關係。本論文旨在以Akt1基因剔除小鼠為模式，探討AKT1在精神分裂症相關表現型以及多巴胺相關行為中之所扮演的角色。本論文的研究包含兩部份，在第一部份的研究中，Akt1基因剔除的公鼠與母鼠在一系列的基本行為測試中大多表現出正常的行為表現，然而相對於控制組，Akt1基因剔除母鼠在尾部懸吊試驗中靜止時間顯著較多，並且有較弱的前脈衝抑制驚跳反應。進一步檢驗與前脈衝抑制驚跳反應相關之聽覺皮質區的綠色螢光標定神經細胞也發現，Akt1基因剔除母鼠的神經細胞形態相較於控制組有顯著的不同。然而藥物測試結果顯示raclopride及clozapine這兩種抗精神分裂症藥物並不能扭轉Akt1基因剔除母鼠的前脈衝抑制驚跳反應缺損，但若使用AKT1下游GSK-3的抑制劑 8-OHDPAT或SB216763，則可以使Akt1 基因剔除母鼠的行為反應恢復到與控制組相近的水準。這部份的研究結果不僅顯示了Akt1基因的缺損的確會影響小鼠在前脈衝抑制驚跳反應的行為以及相關神經細胞形態的表現，且這樣的改變有性別上的差異，此外也凸顯了Akt1基因在多巴胺相關行為中以及藥物遺傳學上對於治療藥物選擇的重要性。在第二部份的研究則利用甲基安非他命引發的行為致敏化及佐以多巴胺類藥物注射為模式，進一步探討AKT1如何調節與多巴胺相關之訊息傳遞。實驗結果顯示，相較於控制組的公鼠，Akt1基因剔除公鼠對於甲基安非他命的致敏化較不敏感，但Akt1基因剔除母鼠和控制組母鼠相比則沒有差異。這樣的性別差異更進一步顯現在同時注射甲基安非他命及多巴胺D2受體致效劑或拮抗劑的甲基安非他命致敏化公鼠的行為，以及利用小動物正子造影技術及18F-FDG量測小鼠腦內紋狀體神經細胞活動情形 上，而甲基安非他命導致之小鼠腦內紋狀體神經細胞活動改變，在注射後的60到90分鐘更加明顯。有趣的是，Akt1基因剔除公鼠在行為致敏化模式下的自主活動量缺損可經由每日注射17β-estradiol的操弄所減緩。這些結果顯示AKT1對 於甲基安非他命致敏化所引發之過度活動的性別差異調控是具有區域性、時間性以及多巴胺D2受體專一性的。綜合以上兩個研究，本論文研究結果支持AKT1參與在多巴胺系統中，並且發現AKT1對多巴胺相關行為表現的影響具有性別上的差異，且雌性激素可能參與其中。 | zh_TW |
| dc.description.abstract | Schizophrenia appears to be a multifactorial disorder and accumulating evidence from human genetic and animal studies suggests that AKT1 (protein kinase Bα) might play certain roles in the pathogenesis of this disorder. Compared with human genetic studies, a mutant mouse model is a simple and relatively straightforward approach for determining the causal relationships and biological functions of AKT1 in the pathogenesis of schizophrenia. This master’s thesis aimed to study the roles of AKT1 in schizophrenia-related phenotypes and dopamine-dependent behaviors using AKT1 mutant mice as a model. In study 1, both male and female Akt1-/- mice displayed normal behavioral profiles in a battery of behavioral tasks but female mutant mice showed sex-specific alterations in immobility in the tail suspension test and in acoustic prepulse inhibition (PPI) compared with their wild-type (WT) controls. Female Akt1-/- mice also exhibited neuromorphological abnormalities in the GFP-labeled pyramidal neurons in the auditory cortex compared with those of the controls. Neither raclopride nor clozapine (antipsychotics) alleviated such PPI deficit in Akt1-/- females but it was mitigated by 8-OH-DPAT and SB216763 (indirect/direct Glycogen synthase kinase 3 (GSK3) inhibitors). The findings in study 1 not only reveal a sex-specific PPI deficit and related neuromorphological alterations in female Akt1-/- mice but also highlight the importance of AKT1 in the dopamine-dependent response and a pharmacogenetic effect of AKT1 on treatment selection. In study 2, the roles of AKT1 in the regulation dopamine signaling are further examined through methamphetamine (Meth)-induced behavioral sensitization and dopaminergic compound challenges. Male Akt1-/- mice were evident to be less sensitive to Meth-induced behavioral sensitization than their WT controls, whereas such genotypic reduction of hyperlocomotion did not appear in females mice. Such sex difference was further observed by co-injections of Meth with dopamine D2 receptor (DRD2) agonist/antagonist (i.e., quinpirole and raclopride) in Meth-sensitized mice and by measuring Meth-induced striatal brain activity using microPET with 18F-FDG, especially 60-90 min after Meth injection. Interestingly, the reduction of Meth-induced behavioral sensitization in Male Akt1-/- mice can be rescued by daily injections of 17β-estradiol. These results suggest a region-specific, temporal-specific and DRD2-specific sex difference of AKT1 in the regulation of Meth-related hyperactivity and estrogen might play some roles in this process. Taken all together, these findings support the involvement of AKT1 in the actions of dopamine and further indicate a sexually dimorphic effect of AKT1 in the regulation of behavioral phenotypes and DA-dependent responses, which might be affected by estrogen. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T04:55:25Z (GMT). No. of bitstreams: 1 ntu-99-R96227115-1.pdf: 14829998 bytes, checksum: 795b3a88161ac519667553f07076d774 (MD5) Previous issue date: 2010 | en |
| dc.description.tableofcontents | Table of Contents
致謝 i 摘要 iii Abstract v Table of Contents vii List of Tables ix List of Figures ix Chapter One : General Introduction 1 1.1. The Overview of Schizophrenia 1 1.2. The Overview of Dopamine 8 1.3. AKTing UP in Schizophrenia 13 1.4. Why Modeling Schizophrenia in Animal Models? 17 1.5. The Objectives of This Thesis 20 Table 21 References 22 Figures 35 Chapter Two : Akt1 Deficiency Causes Sex-Specific Alterations Rescued by GSK3 Inhibitors But Not by Antipsychotic Drugs 41 Abstract 41 Introduction 43 Materials and Methods 45 Results 51 Discussion 54 References 61 Table 69 Figures 70 Appendix: Supplementary Materials 78 Chapter Three : AKTing Up in Mice Reveals Sex Differences in Methamphetamine- Induced Behavioral Sensitization and Striatal Neuron Activity 83 Abstract 83 Introduction 85 Materials and Methods 88 Results 92 Discussion 95 References 101 Table 108 Figures 109 Chapter Four : General Discussion 119 4.1. The Biological Function of AKTs 119 4.2. AKT1 is a Key Signaling Intermediate Downstream of DRD2 121 4.3. AKT1 is Involved in the “Slow Wave of Response” in DA Transmission 121 4.4. The GSK-3, Downstream of AKT, Might Have Therapeutic Potential for Schizophrenia 122 4.5. The Effects of Estrogen in Schizophrenia-related Phenotypes and Dopamine-dependent Behaviors 124 References 127 Figures 130 | |
| dc.language.iso | en | |
| dc.subject | Akt1基因剔除小鼠 | zh_TW |
| dc.subject | 神經細胞形態 | zh_TW |
| dc.subject | GSK-3 抑制劑 | zh_TW |
| dc.subject | 性別差異 | zh_TW |
| dc.subject | 前脈衝抑制驚跳反應 | zh_TW |
| dc.subject | 抗精神分裂症藥物 | zh_TW |
| dc.subject | 甲基安非他命 | zh_TW |
| dc.subject | 正子造影掃描 | zh_TW |
| dc.subject | PET scan | en |
| dc.subject | Akt1 mutant mice | en |
| dc.subject | sex difference | en |
| dc.subject | prepulse inhibition | en |
| dc.subject | antipsychotics | en |
| dc.subject | GSK-3 inhibitor | en |
| dc.subject | neuromorphology | en |
| dc.subject | methamphetamine | en |
| dc.title | 以Akt1基因剔除小鼠為模式檢驗精神分裂症相關表現型以及AKT1對於多巴胺相關行為的影響 | zh_TW |
| dc.title | AKTing Up in Schizophrenia: Examination of Schizophrenia-related Phenotypes and the Involvement of AKT1 in Dopamine-dependent Behaviors Using Akt1 Knockout Mice | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 98-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 何英剛(Ing-Kang Ho),梁庚辰(Keng-Chen Liang),黃宗正(Tzung-Jeng Hwang),陳景宗(Jin-Chung Chen) | |
| dc.subject.keyword | Akt1基因剔除小鼠,性別差異,前脈衝抑制驚跳反應,抗精神分裂症藥物,GSK-3 抑制劑,神經細胞形態,甲基安非他命,正子造影掃描, | zh_TW |
| dc.subject.keyword | Akt1 mutant mice,sex difference,prepulse inhibition,antipsychotics,GSK-3 inhibitor,neuromorphology,methamphetamine,PET scan, | en |
| dc.relation.page | 132 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2010-07-30 | |
| 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 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-99-1.pdf 未授權公開取用 | 14.48 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。