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脑源性神经营养因子、神经营养素-3和神经营养素-4/5可预防亨廷顿舞蹈病啮齿动物模型中纹状体投射神经元的死亡。

Brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 prevent the death of striatal projection neurons in a rodent model of Huntington's disease.

作者信息

Pérez-Navarro E, Canudas A M, Akerund P, Alberch J, Arenas E

机构信息

Departament de Biologia Cel.lular i Anatomia Patològica, Facultat de Medicina, IDIBAPS, Universitat de Barcelona, Spain.

出版信息

J Neurochem. 2000 Nov;75(5):2190-9. doi: 10.1046/j.1471-4159.2000.0752190.x.

Abstract

Intrastriatal injection of quinolinate has been proven to be a very useful animal model to study the pathogenesis and treatment of Huntington's disease. To determine whether growth factors of the neurotrophin family are able to prevent the degeneration of striatal projection neurons, cell lines expressing brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or neurotrophin-4/5 (NT-4/5) were grafted in the adult rat striatum before quinolinate injection. Three days after lesioning, ongoing cell death was assessed by in situ detection of DNA fragmentation. In animals grafted with the control cell line, quinolinate injection induced a gradual cell loss that was differentially prevented by intrastriatal grafting of BDNF-, NT-3-, or NT-415-secreting cells. Seven days after lesioning, we characterized striatal projection neurons that were protected by neurotrophins. Quinolinate injection, alone or in combination with the control cell line, induced a selective loss of striatal projection neurons. Grafting of a BDNF-secreting cell line pre-vented the loss of all types of striatal projection neurons analyzed. Glutamic acid decarboxylase 67-, preproenkephalin-, and preprotachykinin A- but not prodynorphin-expressing neurons were protected by grafting of NT-3- or NT-4/5-secreting cells but with less efficiency than the BDNF-secreting cells. Our findings show that neurotrophins are able to promote the survival of striatal projection neurons in vivo and suggest that BDNF might be beneficial for the treatment of striatonigral degenerative disorders, including Huntington's disease.

摘要

纹状体内注射喹啉酸已被证明是研究亨廷顿病发病机制和治疗方法的一种非常有用的动物模型。为了确定神经营养因子家族的生长因子是否能够预防纹状体投射神经元的退化,在注射喹啉酸之前,将表达脑源性神经营养因子(BDNF)、神经营养因子-3(NT-3)或神经营养因子-4/5(NT-4/5)的细胞系移植到成年大鼠纹状体中。损伤后三天,通过原位检测DNA片段化来评估持续的细胞死亡情况。在移植了对照细胞系的动物中,喹啉酸注射诱导了逐渐的细胞损失,而BDNF、NT-3或NT-4/5分泌细胞的纹状体内移植则以不同方式预防了这种损失。损伤后七天,我们对受神经营养因子保护的纹状体投射神经元进行了特征描述。单独注射喹啉酸或与对照细胞系联合注射,都会导致纹状体投射神经元的选择性损失。移植分泌BDNF的细胞系可预防所分析的所有类型纹状体投射神经元的损失。移植分泌NT-3或NT-4/5的细胞可保护表达谷氨酸脱羧酶67、前脑啡肽原和前速激肽原A但不表达前强啡肽的神经元,但其效率低于分泌BDNF的细胞。我们的研究结果表明,神经营养因子能够促进体内纹状体投射神经元的存活,并提示BDNF可能对治疗包括亨廷顿病在内的纹状体黑质变性疾病有益。

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