Nakata Mariko, Shimoda Masayuki, Yamamoto Shinya
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.
Cereb Cortex Commun. 2021 Feb 1;2(1):tgab006. doi: 10.1093/texcom/tgab006. eCollection 2021.
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.
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。
