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首页> 外文期刊>The European Journal of Neuroscience >Synaptic changes characterize early behavioural signs in the ME7 model of murine prion disease.
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Synaptic changes characterize early behavioural signs in the ME7 model of murine prion disease.

机译：突触的变化表征了小鼠disease病毒ME7模型中的早期行为体征。

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Prion diseases are fatal, chronic neurodegenerative diseases of mammals, characterized by amyloid deposition, astrogliosis, microglial activation, tissue vacuolation and neuronal loss. In the ME7 model of prion disease in the C57BL/6 J mouse, we have shown previously that these animals display behavioural changes that indicate the onset of neuronal dysfunction. The current study examines the neuropathological correlates of these early behavioural changes. After injection of ME7-infected homogenate into the dorsal hippocampus, we found statistically significant impairment of burrowing, nesting and glucose consumption, and increased open field activity at 13 weeks. At this time, microglia activation and PrPSc deposition was visible selectively throughout the limbic system, including the hippocampus, entorhinal cortex, medial and lateral septum, mamillary bodies, dorsal thalamus and, to a lesser degree, in regions of the brainstem. No increase in apoptosis or neuronal cell loss was detectable at this time, while in animals at 19 weeks postinjection there was 40% neuronal loss from CA1. There was a statistically significant reduction in synaptophysin staining in the stratum radiatum of the CA1 at 13 weeks indicating loss of presynaptic terminals. Damage to the dorsal hippocampus is known to disrupt burrowing and nesting behaviour. We have demonstrated a neuropathological correlate of an early behavioural deficit in prion disease and suggest that this should allow insights into the first steps of the neuropathogenesis of prion diseases.
机译：on病毒疾病是哺乳动物的致命性慢性神经退行性疾病，其特征在于淀粉样蛋白沉积，星形胶质增生，小胶质细胞活化，组织空泡化和神经元丢失。在C57BL / 6 J小鼠的pr病毒疾病的ME7模型中，我们先前已证明这些动物表现出行为变化，表明神经元功能异常的发作。当前的研究检查了这些早期行为改变的神经病理学相关性。将ME7感染的匀浆注射入背侧海马后，我们发现穴居，筑巢和葡萄糖消耗有统计学上的显着损害，并在13周时增加了开放野外活动。这时，小胶质细胞激活和PrPSc沉积在整个边缘系统（包括海马，内嗅皮层，内侧和外侧中隔，乳头体，背丘脑以及在较小程度上在脑干区域）可见。此时没有检测到凋亡增加或神经元细胞丢失增加，而在注射后19周的动物中，CA1导致了40％的神经元丢失。在第13周时，CA1放射状层的突触素染色在统计学上显着减少，表明突触前末梢丢失。已知对海马背侧的破坏会破坏穴居和筑巢行为。我们已经证明了病毒病早期行为缺陷的神经病理学相关性，并建议这应允许洞察into病毒病神经发病的第一步。

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