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- Title
Dexmedetomidine Ameliorates Sleep Deprivation-Induced Depressive Behaviors in Mice.
- Authors
Eun-Jin Moon; Il-Gyu Ko; Sung-Eun Kim; Jun-Jang Jin; Lakkyong Hwang; Chang-Ju Kim; Hyeonjun An; Bong-Jae Lee; Jae-Woo Yi
- Abstract
Purpose: Sleep deprivation induces depressive symptoms. Dexmedetomidine is a α2-adrenoreceptor agonist and this drug possesses sedative, anxiolytic, analgesic, and anesthetic-sparing effect. In this study, the action of dexmedetomidine on sleep deprivation-induced depressive behaviors was investigated using mice. Methods: For the inducing of sleep deprivation, the mice were placed inside a water cage containing 15 platforms and filled with water up to 1 cm below the platform surface for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (0.5, 1, and 2 μg/kg) was intraperitoneally treated into the mice, one time per a day during 6 days. Then, forced swimming test and tail suspension test were conducted. Immunohistochemistry for tyrosine hydroxylase (TH), 5-hydroxytryptamine (5-HT; serotonin), tryptophan hydroxylase (TPH) and western blot for D1 dopamine receptor were also performed. Results: Sleep deprivation increased the immobility latency in the forced swimming test and tail suspension test. The expressions of TPH, 5-HT, and D1 dopamine receptor were decreased, whereas, TH expression was increased by sleep deprivation. Dexmedetomidine decreased the immobility latency and increased the expressions of TPH, 5-HT, and D1 dopamine receptor, whereas, HT expression was decreased by dexmedetomidine treatment. Conclusions: In our results, dexmedetomidine alleviated sleep deprivation-induced depressive behaviors by increasing 5-HT synthesis and by decreasing dopamine production with up-regulation of D1 dopamine receptor.
- Subjects
DEXMEDETOMIDINE; MICE behavior; SLEEP deprivation; DOPAMINE receptors; TYROSINE hydroxylase; TRYPTOPHAN; ADRENERGIC receptors
- Publication
International Neurourology Journal, 2018, Vol 22, pS139
- ISSN
2093-4777
- Publication type
Article
- DOI
10.5213/inj.1836228.114