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Photochemically induced thalamus infarction impairs cognition in a mouse model
Stroke and Vascular Neurology ( IF 5.9 ) Pub Date : 2023-12-01 , DOI: 10.1136/svn-2022-002235
Chen Zhang , Shiping Li , Yongjun Wang , Jiong Shi

Background Small subcortical infarcts account for up to 25% of ischaemic strokes. Thalamus is one of the subcortical structures that commonly manifest with lacunar infarcts on MRI of the brain. Studies have shown that thalamus infarction is associated with cognitive decline. However, due to the lack of proper animal models, little is known about the mechanism. We aimed to establish a focal thalamus infarction model, characterise the infarct lesion and assess functional effects. Methods Male C57BL/6J mice were anaesthetised, and Rose Bengal dye was injected through the tail vein. The right thalamus was illuminated with green laser light by stereotactic implantation of optic fibre. Characteristics of the infarct and lesion evolution were evaluated by histological analysis and 7T MRI at various times. The cognitive and neurological functions were assessed by behavioural tests. Retrograde tracing was performed to analyse neural connections. Results An ischaemic lesion with small vessel occlusion was observed in the thalamus. It became a small circumscribed infarct with reactive astrocytes accumulated in the infarct periphery on day 21. The mice with thalamic infarction demonstrated impaired learning and memory without significant neurological deficits. Retrogradely labelled neurons in the retrosplenial granular cortex were reduced. Conclusion This study established a mouse model of thalamic lacunar infarction that exhibits cognitive impairment. Neural connection dysfunctions may play a potential role in post-stroke cognitive impairment. This model helps to clarify the pathophysiology of post-stroke cognitive impairment and to develop potential therapies. Data are available upon reasonable request.

中文翻译:

光化学诱导的丘脑梗塞损害小鼠模型的认知

背景 小型皮质下梗死占缺血性中风的 25%。丘脑是皮质下结构之一,在大脑 MRI 上通常表现为腔隙性梗塞。研究表明,丘脑梗塞与认知能力下降有关。然而,由于缺乏合适的动物模型,人们对其机制知之甚少。我们的目的是建立局灶性丘脑梗死模型,描述梗死病变的特征并评估功能影响。方法将雄性C57BL/6J小鼠麻醉,尾静脉注射玫瑰红染料。通过立体定向植入光纤,用绿色激光照射右侧丘脑。通过组织学分析和7T MRI在不同时间评估梗塞和病变演变的特征。通过行为测试评估认知和神经功能。进行逆行追踪来分析神经连接。结果丘脑出现小血管闭塞的缺血性病变。第 21 天,它变成了一个小的局限性梗塞,反应性星形胶质细胞在梗塞周围积聚。丘脑梗塞的小鼠表现出学习和记忆受损,但没有明显的神经功能缺陷。压后颗粒皮质中逆行标记的神经元减少。结论本研究建立了具有认知障碍的丘脑腔隙性梗塞小鼠模型。神经连接功能障碍可能在中风后认知障碍中发挥潜在作用。该模型有助于阐明中风后认知障碍的病理生理学并开发潜在的治疗方法。数据可根据合理要求提供。
更新日期:2023-12-01
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