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首页> 外文期刊>The European Journal of Neuroscience >Burst-firing patterns in the prefrontal cortex underlying the neuronal mechanisms of depression probed by antidepressants
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Burst-firing patterns in the prefrontal cortex underlying the neuronal mechanisms of depression probed by antidepressants

机译：抗抑郁药探查抑郁神经元机制下前额叶皮层的爆发模式

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Major depressive disorder (MDD) is one of the leading causes of morbidity worldwide. Several antidepressants have been widely prescribed to treat patients with MDD. However, neuronal changes in brain function remain poorly understood. Based on the standard chronic mild stress (CMS) model of depression in mice, we investigated the neuronal mechanisms of the classic antidepressant, fluoxetine, and a new compound (termed YY-23 in this study) derived from furostanol saponin. The results showed that both fluoxetine and YY-23 normalized CMS-induced depressive-like behaviors. YY-23 caused antidepressant-like behaviors with a faster action than fluoxetine. In terms of in vivo neuronal activities, a CMS-induced decrease in spontaneous firing in burst of medial prefrontal cortex pyramidal neurons rather than ventral tegmental area (VTA) was reversed by the chronic administration of fluoxetine and YY-23. We also found that CMS-induced deficits in the expression of prefrontal brain-derived neurotrophic factor (BDNF) were also restored by chronically administering YY-23 and fluoxetine. In addition, chronic administration of fluoxetine rather than YY-23 resulted in an improvement of antidepressive-like behavior and a change of burst firing of VTA in control-housed animals, indicating that the pharmacological effects of YY-23 were specific to CMS-treated animals. Together, these data suggest that the burst-firing patterns of pyramidal cells may be a neural biomarker of depressive-like mice and antidepressant action. Furthermore, synaptic transmission and BDNF may contribute to the rapid antidepressant-like effects on depression.
机译：严重抑郁症（MDD）是全球发病率的主要原因之一。已经广泛开出了几种抗抑郁药来治疗MDD患者。然而，大脑功能的神经元变化仍然知之甚少。基于标准的抑郁症小鼠慢性慢性轻度应激（CMS）模型，我们研究了经典抗抑郁药氟西汀和一种由呋喃固醇皂苷衍生的新化合物（在本研究中称为YY-23）的神经元机制。结果表明，氟西汀和YY-23均使CMS诱导的抑郁样行为正常化。 YY-23导致的抗抑郁样行为比氟西汀更快。就体内神经元活动而言，长期服用氟西汀和YY-23可逆转CMS诱导的内侧前额叶皮层锥体神经元而不是腹侧被盖区（VTA）爆发时自发放电的减少。我们还发现，通过长期服用YY-23和氟西汀，还可以恢复CMS诱导的前额叶脑源性神经营养因子（BDNF）表达的缺陷。此外，氟西汀而非YY-23的长期给药可改善对照组动物的抗抑郁样行为并改变VTA的爆发性放电，这表明YY-23的药理作用对CMS治疗具有特异性动物。总之，这些数据表明锥体细胞的爆发模式可能是抑郁样小鼠和抗抑郁作用的神经生物标记。此外，突触传递和BDNF可能有助于抑郁症的快速抗抑郁样作用。

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