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紫外线诱导的大鼠大脑皮质神经元变性

UV-Induced Neuronal Degeneration in the Rat Cerebral Cortex.

作者信息

Nakata Mariko, Shimoda Masayuki, Yamamoto Shinya

机构信息

Integrative Neuroscience Research Group, Human Informatics and Interaction Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8568, Japan.

Department of Pathology, Keio University School of Medicine, Tokyo 160-8582, Japan.

出版信息

Cereb Cortex Commun. 2021 Feb 1;2(1):tgab006. doi: 10.1093/texcom/tgab006. eCollection 2021.

Abstract

Irradiation with ultraviolet (UV) light on the cortical surface can induce a focal brain lesion (UV lesion) in rodents. In the present study, we investigated the process of establishing a UV lesion. Rats underwent UV irradiation (365-nm wavelength, 2.0 mWh) over the dura, and time-dependent changes in the cortical tissue were analyzed histologically. We found that the majority of neurons in the lesion started to degenerate within 24 h and the rest disappeared within 5 days after irradiation. UV-induced neuronal degeneration progressed in a layer-dependent manner. Moreover, UV-induced terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positivity and heme oxygenase-1 (HO-1) immunoreactivity were also detected. These findings suggest that UV irradiation in the brain can induce gradual neural degeneration and oxidative stress. Importantly, UV vulnerability may vary among cortical layers. UV-induced cell death may be due to apoptosis; however, there remains a possibility that UV-irradiated cells were degenerated via processes other than apoptosis. The UV lesion technique will not only assist in investigating brain function at a targeted site but may also serve as a pathophysiological model of focal brain injury and/or neurodegenerative disorders.

摘要

在啮齿动物的皮质表面用紫外线(UV)照射可诱发局灶性脑损伤(UV损伤)。在本研究中,我们调查了UV损伤的形成过程。对大鼠硬脑膜进行UV照射(波长365 nm,2.0 mWh),并对皮质组织的时间依赖性变化进行组织学分析。我们发现,损伤部位的大多数神经元在照射后24小时内开始退化,其余的在5天内消失。UV诱导的神经元退化呈层依赖性进展。此外,还检测到UV诱导的末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)阳性和血红素加氧酶-1(HO-1)免疫反应性。这些发现表明,大脑中的UV照射可诱导渐进性神经退化和氧化应激。重要的是,UV易损性在不同皮质层之间可能有所不同。UV诱导的细胞死亡可能是由于凋亡;然而,UV照射的细胞仍有可能通过凋亡以外的过程发生退化。UV损伤技术不仅有助于研究目标部位的脑功能,还可能作为局灶性脑损伤和/或神经退行性疾病的病理生理模型。

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