Ji Muhuo, Mao Mingjie, Li Shuming, Zhang Ling, Qiu Lili, Li Bin, Xia Jiangyan, Yang Jianjun
Department of Anesthesiology, Zhongda Hospital, Medical School, Southeast University.
Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing.
Neuroreport. 2019 Apr 10;30(6):421-427. doi: 10.1097/WNR.0000000000001219.
Ketamine has rapid antidepressant effects, but no study to date has investigated changes in resting-state brain activity following ketamine administration in inflammation-induced depression. The purpose of this study was to use blood oxygen level-dependent functional MRI to explore changes in the resting-state brain activity in a rat model of depression induced by lipopolysaccharide (LPS, 1 mg/kg) challenge and to examine whether acute ketamine administration can reverse LPS-induced depressive-like behavior. Here, we showed LPS-induced depressive-like behavior as evidenced by significantly reduced motility in the forced swim test. In addition, LPS-induced increases in plasma levels of proinflammatory cytokines were not completely reversed by acute ketamine administration, suggesting that ketamine exerts its antidepressant effects independently of a possible interference with LPS-induced inflammatory signaling. However, increased regional homogeneity (ReHo) was observed in some brain regions of LPS-exposed animals, including bilateral caudate putamen and nucleus accumbens, which were parts of the mood-regulating circuit. Moreover, ReHo values of bilateral caudate putamen and nucleus accumbens showed significant positive correlations with immobility time. Notably, the LPS-induced depressive-like behavior and increase of ReHo value in the right nucleus accumbens was reversed by acute ketamine administration. In summary, this study suggests that acute ketamine administration is capable of attenuating LPS-induced depressive-like behavior, at least partially by reversing abnormal ReHo in the right nucleus accumbens.
氯胺酮具有快速的抗抑郁作用,但迄今为止尚无研究调查在炎症诱导的抑郁症中给予氯胺酮后静息态脑活动的变化。本研究的目的是使用血氧水平依赖性功能磁共振成像来探索脂多糖(LPS,1mg/kg)激发诱导的抑郁症大鼠模型中静息态脑活动的变化,并检查急性给予氯胺酮是否能逆转LPS诱导的抑郁样行为。在此,我们显示LPS诱导了抑郁样行为,强迫游泳试验中的活动能力显著降低证明了这一点。此外,急性给予氯胺酮并未完全逆转LPS诱导的促炎细胞因子血浆水平升高,这表明氯胺酮发挥其抗抑郁作用独立于对LPS诱导的炎症信号传导的可能干扰。然而,在暴露于LPS的动物的一些脑区观察到区域同质性(ReHo)增加,包括双侧尾状壳核和伏隔核,它们是情绪调节回路的一部分。此外,双侧尾状壳核和伏隔核的ReHo值与不动时间呈显著正相关。值得注意的是,急性给予氯胺酮可逆转LPS诱导的抑郁样行为以及右侧伏隔核中ReHo值的增加。总之,本研究表明急性给予氯胺酮能够减轻LPS诱导的抑郁样行为,至少部分是通过逆转右侧伏隔核中的异常ReHo来实现的。