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两匹患有马退行性脊髓病的阿拉伯马中异常的突触蛋白表达

Abnormal synaptic protein expression in two Arabian horses with equine degenerative myeloencephalopathy.

作者信息

Sisó S, Ferrer I, Pumarola M

机构信息

Priocat Laboratory, Centre de Recerca en Sanitat Animal, Bellaterra Campus, Department of Animal Medicine and Surgery, Veterinary Faculty, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.

出版信息

Vet J. 2003 Nov;166(3):238-43. doi: 10.1016/s1090-0233(02)00302-7.

Abstract

Numerous swollen neurons and multiple dystrophic axons were observed in the gracillis and cuneatus nuclei of two male Arabian horses, aged six and 12 months of age, with equine degenerative myeloencephalopathy. Swollen neurons and dystrophic axons showed synaptophysin, synaptosomal-associated protein of 25 kDa, syntaxin-1 and alpha-synuclein immunoreactivity. Moreover, dystrophic axons were strongly immunopositive against the ubiquitin protein and against the anti-phosphorylated 200 kDa neurofilament protein. Abnormal expression of integral synaptic vesicle, synaptic vesicle-associated presynaptic plasma membrane and cytosolic proteins, which participate in the trafficking, docking and fusion of the synaptic vesicle to the plasma membrane, suggest that severe disruption of axonal transport plays a crucial role in the pathogenesis of dystrophic axons in equine degenerative myeloencephalopathy (EDM).

摘要

在两匹分别为6个月和12个月大的患有马退行性脊髓病的雄性阿拉伯马的薄束核和楔束核中,观察到大量肿胀的神经元和多条营养不良性轴突。肿胀的神经元和营养不良性轴突显示突触素、25 kDa突触体相关蛋白、 syntaxin-1和α-突触核蛋白免疫反应性。此外,营养不良性轴突对泛素蛋白和抗磷酸化200 kDa神经丝蛋白呈强免疫阳性。参与突触小泡向质膜运输、对接和融合途径的完整突触小泡、突触小泡相关突触前质膜和细胞溶质蛋白的异常表达均表明,轴突运输的严重破坏在马退行性脊髓病(EDM)营养不良性轴突的发病机制中起关键作用。

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