异丙酚
焦虑
促肾上腺皮质激素释放激素
高架加迷宫
医学
内科学
神经科学
γ-氨基丁酸受体
内分泌学
激素
心理学
麻醉
受体
精神科
作者
Yu Liu,Xiaona Zhu,Kang Peng,Hong‐Yan Qin,Kexin Yang,Fang Cai,Ji Hu,Ye Zhang
标识
DOI:10.1002/advs.202309059
摘要
Abstract Pain, a comorbidity of anxiety disorders, causes substantial clinical, social, and economic burdens. Emerging evidence suggests that propofol, the most commonly used general anesthetic, may regulate psychological disorders; however, its role in pain‐associated anxiety is not yet described. This study investigates the therapeutic potential of a single dose of propofol (100 mg kg −1 ) in alleviating pain‐associated anxiety and examines the underlying neural mechanisms. In acute and chronic pain models, propofol decreased anxiety‐like behaviors in the elevated plus maze (EPM) and open field (OF) tests. Propofol also reduced the serum levels of stress‐related hormones including corticosterone, corticotropin‐releasing hormone (CRH), and norepinephrine. Fiber photometry recordings indicated that the calcium signaling activity of CRH neurons in the paraventricular nucleus (PVN CRH ) is reduced after propofol treatment. Interestingly, artificially activating PVN CRH neurons through chemogenetics interfered with the anxiety‐reducing effects of propofol. Electrophysiological recordings indicated that propofol decreases the activity of PVN CRH neurons by increasing spontaneous inhibitory postsynaptic currents (sIPSCs). Further, reducing the levels of γ ‐aminobutyric acid type A receptor β 3 (GABA A β 3) subunits in PVN CRH neurons diminished the anxiety‐relieving effects of propofol. In conclusion, this study provides a mechanistic and preclinical rationale to treat pain‐associated anxiety‐like behaviors using a single dose of propofol.
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