High dietary salt intake increases risk of stress-related neuropsychiatric disorders. Here, we explored the contribution of high dietary salt intake-induced neuroinflammation in key stress-responsive brain regions, the hypothalamic paraventricular nucleus and basolateral amygdala, in promoting exaggerated neuronal activation and coping behaviors in response to acute psychogenic stress. Mice that underwent high dietary salt intake exhibited increased active stress coping behaviors during and after an acute swim stress, and these were reduced by concurrent administration of minocycline, an inhibitor of microglial activation, without affecting body fluid hyperosmolality caused by high dietary salt intake. Moreover, minocycline attenuated high dietary salt intake-induced increases of paraventricular nucleus tumor necrosis factor-α, activated microglia (ionized calcium-binding adaptor molecule 1), and acute swim stress-induced neuronal activation (c-Fos). In the basolateral amygdala, similar effects were observed on ionized calcium-binding adaptor molecule 1+ and c-Fos+ counts, but not tumor necrosis factor-α levels. These data indicate that high dietary salt intake promotes neuroinflammation, increasing recruitment of neurons in key stress-associated brain regions and augmenting behavioral hyper-responsivity to acute psychological stress.

译文

:高饮食盐摄入量会增加与压力有​​关的神经精神疾病的风险。在这里,我们探讨了高饮食盐摄入引起的神经炎症在关键的应激反应脑区域,下丘脑室旁核和基底外侧杏仁核中的作用,以促进过度的神经元活化和应对急性精神压力的应对行为。高饮食饮食盐摄入量的小鼠在急性游泳应激期间和之后表现出增加的主动应激应对行为,并且通过同时施用小胶质细胞活化抑制剂米诺环素而减少了这些行为,而不会影响高饮食饮食盐摄入引起的体液高渗。此外,米诺环素减弱高饮食盐摄入量引起的脑室旁核肿瘤坏死因子-α,活化的小胶质细胞(离子化钙结合衔接分子1)和急性游泳应激诱导的神经元活化(c-Fos)的增加。在基底外侧杏仁核中,对电离的钙结合衔接子分子1和c-Fos计数观察到相似的作用,但未观察到肿瘤坏死因子-α水平。这些数据表明,高盐饮食摄入会促进神经炎症,增加关键应激相关脑区神经元的募集,并增强对急性心理应激的行为高反应性。

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