دورية أكاديمية
Dexmedetomidine ameliorates memory impairment in sleep-deprived mice
العنوان: | Dexmedetomidine ameliorates memory impairment in sleep-deprived mice |
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المؤلفون: | Lakkyong Hwang, Il-Gyu Ko, Jun-Jang Jin, Sang-Hoon Kim, Chang-Ju Kim, Boksoon Chang, Jeong Ho Rho, Eun-Jin Moon, Jae-Woo Yi |
المصدر: | Animal Cells and Systems, Vol 23, Iss 6, Pp 371-379 (2019) |
بيانات النشر: | Taylor & Francis Group, 2019. |
سنة النشر: | 2019 |
المجموعة: | LCC:Medicine (General) LCC:Biology (General) |
مصطلحات موضوعية: | sleep deprivation, α2-adrenoceptor agonist, dexmedetomidine, inflammation, memory impairment, Medicine (General), R5-920, Biology (General), QH301-705.5 |
الوصف: | 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. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1976-8354 2151-2485 19768354 10342745 |
Relation: | https://doaj.org/toc/1976-8354; https://doaj.org/toc/2151-2485 |
DOI: | 10.1080/19768354.2019.1688185 |
URL الوصول: | https://doaj.org/article/6970d48da61c4d34a10342745e1acf41 |
رقم الأكسشن: | edsdoj.6970d48da61c4d34a10342745e1acf41 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 19768354 21512485 10342745 |
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DOI: | 10.1080/19768354.2019.1688185 |