1) Kawahara Y, Ito K, Sun H, et al. RNA editing and death of motor neurons. Nature. 2004; 427: 801
|
|
|
2) 日出山拓人, 河原行郎, 郭 伸. ALSとAMPA受容体. 脳神経. 2005; 57: 585-98
|
|
|
3) 郭 伸. ALSの運動ニューロン死とグルタミン酸受容体の分子変化. 神経進歩. 2006; 50: 902-11
|
|
|
4) 五嶋義郎. グルタミン酸受容体の歴史とその背景. Clin Neurosci. 2006; 24: 142-4
|
|
|
5) Rothman SM, Olney JW. Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann Neurol. 1986; 19: 105-11
|
|
|
6) 相澤仁志, 中村良司, 郭 伸. 実験的遅発性興奮性運動ニューロン死. Clin Neurosci. 1998; 16: 58- 62
|
|
|
7) 郭 伸. 興奮性アミノ酸と神経障害-神経疾患の実験動物モデル. In: 後藤文男, 他, 編. AnnaulReview神経 1992. 東京: 中外医学社; 1992. p. 15-30
|
|
|
8) Rothstein JD, Jin L, Dykes-Hoberg M, et al. Chronic inhibition of glutamate uptake produces a model of slow neurotoxicity. Proc. Natl Acad Sci U S A. 1993; 90: 6591-5
|
|
|
9) Hirata A, Nakamura R, Kwak S, et al. AMPA receptor-mediated slow neuronal death in the rat spinal cord induced by long-term blockade of glutamate transporters with THA. Brain Res. 1997; 771: 37-44
|
|
|
10) Carriedo SG, Yin HZ, Weiss JH. Motor neurons are selectively vulnerable to AMPA/kainite receptor-mediated injury in vitro. J Neurosci. 1996; 16: 4069-79
|
|
|
11) Nakamura R, Kamakura K, Kwak S. Late-onset selective neuronal damage in the rat spinal cord induced by continuous intrathecal administration of AMPA. Brain Research. 1994; 654: 279-85
|
|
|
12) Sun H, Kawahara Y, Ito K, et al. Slow and selective death of spinal motor neurons in vivo by intrathecal infusion of kainic acid: implications for AMPA receptor-mediated excitotoxicity in ALS. J Neurochem. 2006; 98: 782-91
|
|
|
13) 鈴木岳之, 都築馨介, 亀山仁彦, 他. AMPA受容体の生理機能-受容体機能発現から疾患まで-. 日薬理誌. 2003; 122: 515-26
|
|
|
14) 小澤瀞司. 中枢神経系のグルタミン酸受容体, 脳神経. 2001; 53: 605-15
|
|
|
15) Vennekens R, Voets T, Bindels RJ, et al. Current understanding of mammalian TRP homologues. Cell Calcium. 2002; 31: 253-64
|
|
|
16) Kawahara Y, Kwak S. Excitatotoxicity and ALS: What is unique about the AMPA receptors expressed on spinal motor neurons ? Amyotrophic lateral sclerosis. 2005; 1-14
|
|
|
17) 日出山拓人, 河原行郎, 郭 伸. 筋萎縮性側索硬化症の分子病理~病態と治療~. 最新医学. 2005; 60: 1072-82
|
|
|
18) 日出山拓人, 河原行郎, 郭 伸. 筋萎縮性側索硬化症の研究の進歩. 医学のあゆみ. 2005; 212: 2613-20
|
|
|
19) Kwak S, Kawahara Y. Deficient RNA editing of GluR2 and neuronal death in ALS. J Mol Med. 2005; 83: 110-20
|
|
|
20) 崎村建司. AMPA型グルタミン酸受容体の構造と機能. Clin Neurosci. 2006; 24: 145-8
|
|
|
21) Hollmann M, Hartley M, Heinemann S. Ca2+ permeability of KA-AMPA--gated glutamate receptor channels depends on subunit composition. Science. 1991; 252: 851-3
|
|
|
22) Verdoorn TA, Burnashev N, Monyer H, et al. Structural determinants of ion flow through recombinant glutamate receptor channels. Science. 1991; 252: 1715-8
|
|
|
23) Burnashev N, Khodorova A, Jonas P, et al. Calcium-permeable AMPA-kainate receptors in fusiform cerebellar glial cells. Science. 1992; 256: 1566-70
|
|
|
24) Nutt S, Kamboj R. Differential RNA editing efficiency of AMPA receptor subunit GluR-2 in human brain. Neuroreport. 1994; 5: 1679-83
|
|
|
25) Geiger JR, Melcher T, Koh DS, et al. Relative abundance of subunit mRNAs determines gating and Ca2+ permeability of AMPA receptors in principal neurons and interneurons in rat CNS. Neuron. 1995; 15: 193-204
|
|
|
26) Higuchi M, Single FN, Kohler M, et al. RNA editing of AMPA receptor subunit GluR-B: a base-paired intron-exon structure determines position and efficiency. Cell. 1993; 75: 1361-70
|
|
|
27) Sommer B, Kohler M, Sprengel R, et al. RNA editing in brain controls a determinant of ion flow in glutamate-gated channels. Cell. 2001; 67: 11-9
|
|
|
28) Rueter SM, Dawson TR, Emeson RB. Regulation of alternative splicing by RNA editing. Nature. 1999; 399: 75-80
|
|
|
29) Koh DS, Burnashev N, Jonas P. Block of native Ca2+-permeable AMPA receptors in rat brain by intracellular polyamines generates double rectification. J Physiol. 1995; 486: 305-12
|
|
|
30) Jia Z, Agopyan N, Miu P, et al. Enhanced LTP in mice deficient in the AMPA receptor GluR2. Neuron. 1996; 17: 945-56
|
|
|
31) Brusa R, Zimmermann F, Koh DS, et al. Early-onset epilepsy and postnatal lethality associated with an editing-deficient Glu R-B allele in mice. Science. 1995; 270: 1677-80
|
|
|
32) Greger IH, Khatri L, Kong X, et al. AMPA receptor tetramerization is mediated by Q/R editing. Neuron. 2003; 40: 763-74
|
|
|
33) Greger IH, Khatri L, Ziff EB. RNA editing at arg607 controls AMPA receptor exit from the endoplasmic reticulum. Neuron. 2002; 34: 759-72
|
|
|
34) Mahajan SS, Ziff EB. Novel toxicity of the unedited GluR2 AMPA receptor subunit dependent on surface trafficking and increased Ca2+-permeability. Mol Cell Neurosci. 2007; 35: 470-81
|
|
|
35) Kawahara Y, Kwak S, Sun H, et al. Human spinal mononeurons express low relative abundance of GluR2 mRNA: an implication for excitotoxicity in ALS. J Neurochem. 2003; 85: 680-9
|
|
|
36) Takuma H, Kwak S, Yoshizawa T, et al. Reduction of GluR2 RNA editing, a molecular change that increases calcium influx through AMPA receptors, selective in the spinal ventral gray of patients with amyotrophic lateral sclerosis. Ann Neurol. 1999; 46: 806-15
|
|
|
37) Aizawa H, Kimura T, Hashimoto K, et al. Basophilic cytoplasmic inclusions in a case of sporadic juvenile amyotrophic lateral sclerosis. J Neurol Sci. 2000; 176: 106-13
|
|
|
38) 郭 伸, 日出山拓人, 西本祥仁, 他. 孤発性ALSの脊髄前角におけるRNA編集異常と病型. 厚生労働科学研究費補助金難治性疾患克服研究事業神経変性疾患に関する調査研究班報告書. 2007. p. 64-5
|
|
|
39) Kawahara Y, Sun H, Ito K, et al. Underediting of GluR2 mRNA, a neuronal death inducing molecular change in sporadic ALS, does not occur in motor neurons in ALS1 or SBMA. Neurosci Res. 2006; 54: 11-4
|
|
|
40) Van Damme P, Braeken G, Callewaert G, et al. GluR2 deficiency accelerates motor neuron degeneration in a mouse model of amyotrophic lateral sclerosis. J Neuropathol Exp Neurol. 2005; 64: 605-12
|
|
|
41) Kuner R, Groom AJ, Bresink I, et al. Late-onset motoneuron disease caused by a functionally modeified AMPA receptor subunit. Proc Natl Acad Sci U S A. 2005; 102: 5826-31
|
|
|
42) Tateno M, Sadakata H, Tanaka M, et al. Calcium-permeable AMPA receptors promote misfolding of mutant SOD1 protein and development of amyotrophic lateral sclerosis in a transgenic mouse model. Hum Mol Genet. 22004; 13: 2183-96
|
|
|
43) Spalloni A, Albo F, Ferrari F, et al. Cu/Zn-superoxide dismutase(GLY93-->ALA) mutation alters AMPA receptor subunit expression and function and potentiates kainite-mediated toxicity in motor neurons in culture. Neurobiol Dis. 2004; 15: 340-50
|
|
|
44) Tortarolo M, Grignaschi G, Calvaresi N, et al. Glutamate AMPA receptors change in motor neurons of SOD1G93A transgenic mice and their inhibition by a noncompetitive antagonist ameliorates the progression of amyotrophic lateral sclerosis-like disease. J Neurosci Res. 2006; 83: 134-46
|
|
|
45) Sun H, Kawahara Y, Ito K, et al. Slow and selective death of spinal motor neurons in vivo by intrathecal infusion of kainic acid: implications for AMPA receptor-mediated excitotoxicity in ALS. J Neurochem. 2006; 98: 782-91
|
|
|
46) Mackenzie IR, Bigio EH, Ince PG, et al. Pathological TDP-43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations. Ann Neurol. 2007; 61: 427-34
|
|
|
47) Tan CF, Eguchi H, Tagawa A, et al. TDP-43 immunoreactivity in neuronal inclusions in familial amyotrophic lateral sclerosis with or without SOD1 gene mutation. Acta Neuropathol. 2007; 113: 535-42
|
|
|
48) Levine MS, Klapstein GJ, Koppel A, et al. Enhanced sensitivity of N-methyl-D-aspartate receptor activation in transgenic and knockin mouse models of Huntington's disease. J Neurosci Res. 1999; 58: 515-32
|
|
|
49) Morton AJ, Leavens W. Mice transgenic for the human Huntington's disasese mutation have reduced sensitivity to kainic acid toxicity. Brain Res Bull. 2006; 52: 51-9
|
|
|
50) Snider BJ, Moss JL, Revilla FJ, et al. Neocortical neurons cultured from mice with expanded CAG repeats in the huntingtin gene: unaltered vulnerability to excitotoxins and other insults. Neuroscience. 2003; 120: 617-25
|
|
|
51) Zeron MM, Hansson O, Chen N, et al. Increased sensitivity to N-methyl-D-aspartate receptor-mediated excitotoxicity in a mouse model of Huntington's disease. Neuron. 2002; 33: 849-60
|
|
|
52) Kwak S, Weiss JH. Calcium-permeable AMPA channel in neurodegenerative disease and ischemia. Curr Opin Neurobiol. 2006; 16: 281-7
|
|
|
53) Sun H, Kawahara Y, Ito K, et al. Expression profile of AMPA receptor subunit mRNA in single adult rat brain and spinal cord neurons in situ. Neurosci Res. 2005; 52: 228-34
|
|
|
54) Higuchi M, Maas S, Single FN, et al. Point mutation in an AMPA recepotor gene rescues lethality in mice deficient in the RNA-editing enzyme ADAR2. Nature. 2000; 406: 78-81
|
|
|
55) Kawahara Y, Ito K, Sun H, et al. Regulation of glutamate receptor RNA editing and ADAR mRNA expression in developing human normal and Down's syndrome brains. Dev Brain Res. 2004; 148: 151-5
|
|
|
56) Kawahara Y, Ito K, Sun H, et al. Low editing efficiency of GluR2 mRNA is associated with a low relative abundant of ADAR2 mRNA in white matter of normal human brain. Eur J Neurosci. 2003; 18: 23-33
|
|
|