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突触蛋白与神经系统疾病 被引量:1

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摘要 突触蛋白是一组与突触相关的具有神经元特异性的磷酸蛋白,突触蛋白在调节神经递质的释放和神经元的早期发育、再生等方面起着重要的作用。脑缺血缺氧、Alzheimer病、朊蛋白病和癫痫等神经系统疾病均存在突触蛋白表达的改变,研究突触蛋白表达的改变是研究这些神经系统疾病的发病机制、病理及生理改变的重要手段。
出处 《国外医学(神经病学.神经外科学分册)》 2004年第1期94-97,共4页 Foreign Medical Sciences(Section On Neurology & Neurosurgery)
基金 国家自然科学基金(30070825)
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  • 1Bustos R, Kolen ER, Braiterman L, et al. Synapsin I is expressed in epithelial cells: localization to a unique trans - Golgi compartment. J Cell Sci, 2001, ll4(Pt 20) : 3695 - 3704.
  • 2Jovanovie jN, Sihra TS, Naim AC, et al. Opposing changes in phosphorylation of specific sites in synapsin I during Ca2 + - dependent glutamate release in isolated nerve terminals. J Neurosci, 2001, 21(20) : 7944 - 7953.
  • 3Leypoldt F, Flajolet M, Methner A. Neuronal differentiation of cultured human NTERA - 2cl. DI cells leads to increased expression of synapsins. Neurosei Lett, 2002, 324(1): 37-40.
  • 4Mozhayeva MG, Sara Y, Liu X, et al. Development of vesicle pools during maturation of hippocampal synapse. J Neurosci, 2002, 22(3):654 - 665.
  • 5Marti E, Ferrer I, Blasi J. Transient increase of synapsin-I immunoreactivity in the mossy fiber layer of the hippocampus after transient forebrain ischemia in the Mongolian gerbil. Brain Res, 1999,824(2) : 153 - 160.
  • 6Bernabeu R, Sharp FR. NMDA and AMPA/kainite glutamate receptors modulate dentate neurogenesis and CA3 syrmpsin - I in normal and ischemic hippocampus. J Cereb Blood Flow Metab, 2000, 20( 12):1669- 1680.
  • 7Bolay H, Gursoy - Ozdemir Y, Sara Y, et al. Persistent defect in transmitter release and synapsin phosphorylation in cerebral cortex after transient moderate ischemic injury. Stroke, 2002, 33( 10): 1369-1375.
  • 8Moretto MB, de Matto - Durra A, Arteni N, et al. Effects of neonatal cerebral hypoxia - ischemia on the in vitro phosphorylation of synapsin-I in rat synaptosomes. Neurachem Res, 1999, 24(10) : 1263 - 1269.
  • 9Ho L, Guo Y, Spielman L, et al. Altered expression of a - type but not b-type synapsin isoform in the brain of patients at high risk for Alzheimer' s disease assessed by DNA microarray technique. Neurosci Lett, 2001, 298(3): 191 - 194.
  • 10Fetter I, Marti E, Tortosa A, et al. Dystrophic neurites of senile plaques are defective in protein involved in exocytosis and neurotransmission. J Neuropathol Exp Neurol, 1998, 57(3): 218-225.

同被引文献33

  • 1梁燕玲,张苏明,许康.短暂脑缺血再灌流后大鼠突触蛋白-I的表达及其磷酸化水平[J].中风与神经疾病杂志,2004,21(3):196-198. 被引量:3
  • 2Iwakuma M,Anzai T,Kobayashi S,et al.Antisense in vivo knockdowm of synaptotagmin I and synapsin I by HVJ-liposome mediated gene transfer modulates ischemic injury of hippocampus in opposing ways.Neurosci Res2003;45(3):285-96.
  • 3Hilfiker S,Pierbone VA,Czzerinik AJ,et al.Synapsins as regulators of neurotransmitter release.Philos Trans R Soc Lond B Biol Sci 1999;354(1381):269-79.
  • 4Roman GC.Vascular dementia may be the most common form of dementia in the elderly.J Neurol Sci 2002;203-204(15):7-10.
  • 5Ford GA,Bryant CA,Mangoni AA,et al.Stroke,dementia,and drug delivery.Br J Clin Pharmacol 2004;57(1):15-26.
  • 6Masliah E.Recent advances in the understanding of the role of synaptic proteins in Alzheimer's Disease and other neurodegenerative disorders.J Alzheimer's Disease 2001:3:121-9.
  • 7Kovalenko TM,Osadchenko IO,Smozhanyk KH,et al.Structural orgamization of CA1 zone in the hippocampus of rats in the experimental brain ischemia.Fiziol ZH 2004:50(2):86-93.
  • 8Martone ME,jones YZ,Young SJ et al.Modification of postsynaptic densities after transient cerebral ischemia:a quantitative and three-dimensional ultrastructural study.J Neurosci 1999;19(6):1988-97.
  • 9Tang YP,Shimizu E,Dube GR,et al.Genetic enhancement of learning and memory in mice.Nature 1999;401(2):63-9.
  • 10Remondes M,Schuman EM.Molecular mechanisms contributing to long-lasting synaptic plasticity at the temporoammonic-CA1 synapse.Learn Mem 2003;10(4):247-52.

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