イシヅカ　ユウタ   Yuta Ishizuka   石塚　佑太    所属   川崎医科大学  医学部 基礎医学　病態代謝学    職種   講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	X Irradiation Induces Acute Cognitive Decline via Transient Synaptic Dysfunction.
掲載誌名	正式名：Radiation research 略　 称：Radiat Res ISSNコード：19385404/00337587
掲載区分	国外
出版社	ALLEN PRESS
巻・号・頁	185(4),pp.423-30
著者・共著者	Anggraeini Puspitasari, Noriko Koganezawa, Yuta Ishizuka, Nobuhiko Kojima, Natsume Tanaka, Takashi Nakano, Tomoaki Shirao*
発行年月	2016/04
概要	Cranial X irradiation can severely impair higher brain function, resulting in neurocognitive deficits. Radiation-induced brain injury is characterized by acute, early and late delayed changes, and morbidity is evident more than 6 months after irradiation. While the acute effects of radiation exposure on the brain are known, the underlying mechanisms remain unclear. In this study, we examined the acute effect of X radiation on synaptic function using behavioral analysis and immunohistochemistry. We found that 10 Gy whole-brain irradiation immediately after conditioning (within 30 min) impaired the formation of fear memory, whereas irradiation 24 h prior to conditioning did not. To investigate the mechanisms underlying these behavioral changes, we irradiated one hemisphere of the brain and analyzed synaptic function and adult neurogenesis immunohistochemically. We focused on drebrin, whose loss from dendritic spines is a surrogate marker of synaptopathy. The intensity of drebrin immunoreactivity started to decrease in the irradiated hemisphere 2 h after exposure. The immunostaining intensity recovered to preirradiation levels by 24 h, indicating that X radiation induced transient synaptic dysfunction. Interestingly, the number of newly generated neurons was not changed at 2 h postirradiation, whereas it was significantly decreased at 8 and 24 h postirradiation. Because irradiation 24 h prior to conditioning had no effect on fear memory, our findings suggest that radiation-induced death of newly-generated neurons does not substantially impact fear memory formation. The radiation-induced synaptic dysfunction likely caused a transient memory deficit during the critical period for fear memory formation (approximately 1-3 h after conditioning), which coincides with a change in drebrin immunostaining in the hippocampus, a structure critical for fear memory formation.
DOI	10.1667/RR14236.1
PMID	27023259