文献リスト

1）Penzes P, Cahill ME, Jones KA, et al. Dendritic spine pathology in neuropsychiatric disorders. Nat Neurosci. 2011; 14: 285-93

2）Cesa R, Strata P. Axonal competition in the synaptic wiring of the cerebellar cortex during development and in the mature cerebellum. Neuroscience. 2009; 162: 624-32

3）Holtmaat A, Svoboda K. Experience-dependent structural synaptic plasticity in the mammalian brain. Nat Rev Neurosci. 2009; 10: 647-58

4）Brose N, OʼConnor V, Skehel P. Synaptopathy: dysfunction of synaptic function? Biochem Soc Trans. 2010; 38: 443-4

5）Yuzaki M. Cbln and C1q family proteins: new transneuronal cytokines. Cell Mol Life Sci. 2008; 65: 1698-705

6）柚﨑通介．シナプス形成・維持を制御する新しいサイトカイン－CblnとC1q/TNFスーパーファミリー．Brain Medical. 2008; 20: 41-6

7）Stephan AH, Barres BA, Stevens B. The complement system: an unexpected role in synaptic pruning during development and disease. Annu Rev Neurosci. 2012; 35: 369-89

8）Song J, Lee JE. Adiponectin as a new paradigm for approaching Alzheimerʼs disease. Anat Cell Biol. 2013; 46: 229-34

9）Boulanger LM. Immune proteins in brain development and synaptic plasticity. Neuron. 2009; 64: 93-109

10）Perry VH, OʼConnor V. C1q: the perfect complement for a synaptic feast? Nat Rev Neurosci. 2008; 9: 807-11

11）Ghai R, Waters P, Roumenina LT, et al. C1q and its growing family. Immunobiology. 2007; 212: 253-66

12）Kishore U, Gaboriaud C, Waters P, et al. C1q and tumor necrosis factor superfamily: modularity and versatility. Trends Immunol. 2004; 25: 551-61

13）Kouser L, Madhukaran SP, Shastri A, et al. Emerging and Novel Functions of Complement Protein C1q. Front Immunol. 2015; 6: 317

14）Bao D, Pang Z, Morgan JI. The structure and proteolytic processing of Cbln1 complexes. J Neurochem. 2005; 95: 618-29

15）Iijima T, Miura E, Matsuda K, et al. Characterization of a transneuronal cytokine family Cbln--regulation of secretion by heteromeric assembly. Eur J Neurosci. 2007; 25: 1049-57

16）Miura E, Iijima T, Yuzaki M, et al. Distinct expression of Cbln family mRNAs in developing and adult mouse brains. Eur J Neurosci. 2006; 24: 750-60

17）Hirai H, Pang Z, Bao D, et al. Cbln1 is essential for synaptic integrity and plasticity in the cerebellum. Nat Neurosci. 2005; 8: 1534-41

18）Ito M. Cerebellar circuitry as a neuronal machine. Prog Neurobiol. 2006; 78: 272-303

19）Ito M. Error detection and representation in the olivo-cerebellar system. Front Neural Circuits. 2013; 7: 1-8

20）Emi K, Kakegawa W, Miura E, et al. Reevaluation of the role of parallel fiber synapses in delay eyeblink conditioning in mice using Cbln1 as a tool. Front Neural Circuits. 2013; 7: 180

21）掛川　渉，幸田和久，柚﨑通介．シナプスを形成するばかりじゃない－δ2型グルタミン酸受容体とCbln1による新しいシナプス可塑性機構．脳21. 2013; 16: 261-9

22）Ito-Ishida A, Miura E, Emi K, et al. Cbln1 regulates rapid formation and maintenance of excitatory synapses in mature cerebellar Purkinje cells in vitro and in vivo. J Neurosci. 2008; 28: 5920-30

23）Yuzaki M. The ins and outs of GluD2--why and how Purkinje cells use the special glutamate receptor. Cerebellum. 2012; 11: 438-9

24）Matsuda K, Miura E, Miyazaki T, et al. Cbln1 is a ligand for an orphan glutamate receptor delta2, a bidirectional synapse organizer. Science. 2010; 328: 363-8

25）Kashiwabuchi N, Ikeda K, Araki K, et al. Impairment of motor coordination, Purkinje cell synapse formation, and cerebellar long-term depression in GluR delta 2 mutant mice. Cell. 1995; 81: 245-52

26）Matsuda K, Yuzaki M. Cbln family proteins promote synapse formation by regulating distinct neurexin signaling pathways in various brain regions. Eur J Neurosci. 2011; 33: 1447-61

27）Uemura T, Lee SJ, Yasumura M, et al. Trans-synaptic interaction of GluRdelta2 and Neurexin through Cbln1 mediates synapse formation in the cerebellum. Cell. 2010; 141: 1068-79

28）Yuzaki M. Cbln1 and its family proteins in synapse formation and maintenance. Curr Opin Neurobiol. 2011; 21: 215-20

29）Kavety B, Jenkins NA, Fletcher CF, et al. Genomic structure and mapping of precerebellin and a precerebellin-related gene. Brain Res Mol Brain Res. 1994; 27: 152-6

30）Rong Y, Wei P, Parris J, et al. Comparison of Cbln1 and Cbln2 functions using transgenic and knockout mice. J Neurochem. 2012; 120: 528-40

31）Konno K, Matsuda K, Nakamoto C, et al. Enriched expression of GluD1 in higher brain regions and its involvement in parallel fiber-interneuron synapse formation in the cerebellum. J Neurosci. 2014; 34: 7412-24

32）Pang Z, Zuo J, Morgan JI. Cbln3, a novel member of the precerebellin family that binds specifically to Cbln1. J Neurosci. 2000; 20: 6333-9

33）Bao D, Pang Z, Morgan MA, et al. Cbln1 is essential for interaction-dependent secretion of Cbln3. Mol Cell Biol. 2006; 26: 9327-37

34）Miura E, Matsuda K, Morgan JI, et al. Cbln1 accumulates and colocalizes with Cbln3 and GluRdelta2 at parallel fiber-Purkinje cell synapses in the mouse cerebellum. Eur J Neurosci. 2009; 29: 693-706

35）Joo JY, Lee SJ, Uemura T, et al. Differential interactions of cerebellin precursor protein (Cbln) subtypes and neurexin variants for synapse formation of cortical neurons. Biochem Biophys Res Commun. 2011; 406: 627-32

36）Haddick PC, Tom I, Luis E, et al. Defining the ligand specificity of the deleted in colorectal cancer (DCC) receptor. PLoS One. 2014; 9: e84823

37）Wei P, Pattarini R, Rong Y, et al. The Cbln family of proteins interact with multiple signaling pathways. J Neurochem. 2012; 121: 717-29

38）Fazeli A, Dickinson SL, Hermiston ML, et al. Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene. Nature. 1997; 386: 796-804

39）Kakegawa W, Mitakidis N, Miura E, et al. Anterograde C1ql1 signaling is required in order to determine and maintain a single-winner climbing fiber in the mouse cerebellum. Neuron. 2015; 85: 316-29

40）Iijima T, Miura E, Watanabe M, et al. Distinct expression of C1q-like family mRNAs in mouse brain and biochemical characterization of their encoded proteins. Eur J Neurosci. 2010; 31: 1606-15

41）Kano M, Hashimoto K. Synapse elimination in the central nervous system. Curr Opin Neurobiol. 2009; 19: 154-61

42）Watanabe M, Kano M. Climbing fiber synapse elimination in cerebellar Purkinje cells. Eur J Neurosci. 2011; 34: 1697-710

43）Bolliger MF, Martinelli DC, Südhof TC. The cell-adhesion G protein-coupled receptor BAI3 is a high-affinity receptor for C1q-like proteins. Proc Natl Acad Sci U S A. 2011; 108: 2534-9

44）Shimono C, Manabe R, Yamada T, et al. Identification and characterization of nCLP2, a novel C1q family protein expressed in the central nervous system. J Biochem. 2010; 147: 565-79

45）Clarke RA, Lee S, Eapen V. Pathogenetic model for Tourette syndrome delineates overlap with related neurodevelopmental disorders including Autism. Transl Psychiatry. 2012; 2: e158

46）Gazzellone MJ, Zhou X, Lionel AC, et al. Copy number variation in Han Chinese individuals with autism spectrum disorder. J Neurodev Disord. 2014; 6: 34

47）Greenwood TA, Light GA, Swerdlow NR, et al. Association analysis of 94 candidate genes and schizophrenia-related endophenotypes. PLoS One. 2012; 7: e29630

48）Jones RM, Cadby G, Melton PE, et al. Genome-wide association study of autistic-like traits in a general population study of young adults. Front Hum Neurosci. 2013; 7: 658

49）Lanoue V, Usardi A, Sigoillot SM, et al. The adhesion-GPCR BAI3, a gene linked to psychiatric disorders, regulates dendrite morphogenesis in neurons. Mol Psychiatry. 2013; 18: 943-50

50）Takao K, Kobayashi K, Hagihara H, et al. Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia. Neuropsychopharmacology. 2013; 38: 1409-25

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