Dexmedetomidine ameliorates memory impairment in sleep-deprived mice
황락경, 고일규, 진준장, 김상훈, 김장주, 장복순, 노정호, 문은진, 이재우,
소속 상세정보
황락경 ( Hwang Lak-Kyong ) - Kyung Hee University College of Medicine Department of Physiology
고일규 ( Ko Il-Gyu ) - Kyung Hee University College of Medicine Department of Physiology
진준장 ( Jin Jun-Jang ) - Kyung Hee University College of Medicine Department of Physiology
김상훈 ( Kim Sang-Hoon ) - Kyung Hee University College of Medicine Department of Physiology
김장주 ( Kim Chang-Ju ) - Kyung Hee University College of Medicine Department of Physiology
장복순 ( Chang Bok-soon ) - Kyung Hee University Hospital at Gangdong Department of Pulmonary and Critical Care Medicine
노정호 ( Rho Jeong-Ho ) - Kyung Hee University Graduate School Department of Medicine
문은진 ( Moon Eun-Jin ) - Kyung Hee University Hospital at Gangdong Department of Anesthesiology and Pain Medicine
이재우 ( Yi Jae-Woo ) - Kyung Hee University Hospital at Gangdong Department of Anesthesiology and Pain Medicine
Abstract
The selective α2-adrenergic receptor agonist dexmedetomidine acts as an analgesic, sedative, and anesthetic adjuvant. The most common consequence of sleep deprivation is memory impairment. We investigated whether dexmedetomidine can counteract memory impairment caused by sleep deprivation and suppress the production of inflammatory factors. For inducing sleep deprivation, adult male mice were placed inside a water cage containing 15 platforms immersed in water up to 1?cm for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (5, 10, and 20?μg/kg) and α2-adrenoceptor antagonist atipamezole (250?μg/kg) were intraperitoneally injected into the mice, once per day for six days. The step-down avoidance task and the Morris water maze test were performed. Western blot analysis was performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, brain-derived neurotrophic factor (BDNF), tyrosine kinase B (TrkB), nuclear transcription factor-κB (NF-κB), inhibitor of κBα (IκBα), and ionized calcium binding adapter molecule I (Iba-1) in the hippocampus. Immunohistochemistry was performed for the determination of Ki-67 and glial fibrillary acidic protein (GFAP) expression in the hippocampal dentate gyrus. Dexmedetomidine ameliorated sleep deprivation-induced deterioration of short-term memory and spatial learning ability. Dexmedetomidine inhibited production of inflammatory mediators caused by sleep deprivation. Dexmedetomidine also prevented the decrease in BDNF, TrkB expression, and cell proliferation induced by sleep deprivation. Dexmedetomidine could be used to counteract the neuropathological effects of sleep deprivation.
키워드
Sleep deprivation; α2-adrenoceptor agonist; dexmedetomidine; inflammation; memory impairment
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