右美托咪定
医学
抗焦虑药
开阔地
高架加迷宫
育亨宾
焦虑
内科学
内分泌学
下丘脑
麻醉
药理学
敌手
神经科学
受体
精神科
生物
镇静
作者
Gaolin Qiu,Peng Wang,Jun Rao,Xin Qing,Chenchen Cao,Dijia Wang,Bin Mei,Jiqian Zhang,Liu Hu,Zhilai Yang,Xuesheng Liu
出处
期刊:Anesthesiology
[Ovid Technologies (Wolters Kluwer)]
日期:2024-03-18
被引量:1
标识
DOI:10.1097/aln.0000000000004982
摘要
Dexmedetomidine has repeatedly shown to improve anxiety but the precise neural mechanisms underlying this effect remain incompletely understood. Here, we aim to explore the role of corticotropin-releasing hormone-producing hypothalamic paraventricular (CRHPVN) neurons in mediating the anxiolytic effects of dexmedetomidine.A social defeat stress mouse model was employed to evaluate the anxiolytic effects induced by dexmedetomidine through the elevated plus-maze, open-field test, and measurement of serum stress hormone levels. In vivo Ca2+ signal fibre photometry and ex vivo patch-clamp recordings were utilized to determine the excitability of CRHPVN neurons and investigate the specific mechanism involved. CRHPVN neuron modulation was achieved through chemogenetic activation or inhibition.Compared with saline, dexmedetomidine (40 µg/kg) alleviated anxiety-like behaviors. Additionally, dexmedetomidine reduced CRHPVN neuronal excitability. Chemogenetic activation of CRHPVN neurons decreased the time spent in the open arms of the elevated plus-maze and in the central area of the open-field test. Conversely, chemogenetic inhibition of CRHPVN neurons had the opposite effect. Moreover, the suppressive impact of dexmedetomidine on CRHPVN neurons was attenuated by the α2 receptor antagonist yohimbine.Our results indicate that the anxiety-like effects of dexmedetomidine are mediated via α2 adrenergic receptor-triggered inhibition of CRHPVN neuronal excitability in the hypothalamus.
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