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首页> 外文期刊>The journal of clinical psychiatry >Atypical antipsychotics in bipolar depression: potential mechanisms of action.
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Atypical antipsychotics in bipolar depression: potential mechanisms of action.

机译：双相抑郁症的非典型抗精神病药：潜在的作用机制。

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"Conventional" antidepressants, such as the selective serotonin reuptake inhibitors (SSRIs), bupropion, or serotonin-norepinephrine reuptake inhibitors, are not recommended as monotherapy for bipolar depression. Although they are likely to provide effective symptom relief in combination with mood stabilizers, the risk of precipitating a switch to mania often complicates their use even as combination therapy. Recently, 2 psychotropic medications approved for treating acute mania, olanzapine and quetiapine, have also been shown to possess antidepressant activity without destabilizing mood and, as such, are potential mood stabilizers. This article aims to review the mechanism of action of conventional antidepressants and newer agents that are effective in the treatment of bipolar depression. A number of mechanisms have been postulated to play a role in the effective treatment of bipolar depression, including targets as diverse as serotonin (5-HT), norepinephrine, dopamine, gamma-aminobutyric acid (GABA), glutamate, and various second messenger signaling pathways. A review of the data reveals an important point of commonality among the antidepressant treatments, olanzapine, and quetiapine. Antidepressant treatments, such as norepinephrine reuptake inhibitors, SSRIs, and electroconvulsive therapy, induce a reduction of 5-HT(2A) receptors. Both olanzapine and quetiapine not only are antagonists at this receptor but also induce downregulation of 5-HT(2A) receptors. It is possible that the antidepressant efficacy of these agents is mediated by this receptor, while the additional benefit of olanzapine and quetiapine over unimodal antidepressant treatments, in terms of stabilizing mood, may be provided by their concomitant dopamine D(2) antagonism. Further studies should be conducted to examine these hypotheses.
机译：不推荐将“常规”抗抑郁药（例如选择性5-羟色胺再摄取抑制剂（SSRIs），安非他酮或5-羟色胺-去甲肾上腺素再摄取抑制剂）作为双相抑郁的单一疗法。尽管它们可能与情绪稳定剂联合使用可提供有效的症状缓解，但诱发躁狂症的风险通常会使它们的使用变得复杂，即使将其用作联合治疗也是如此。最近，还显示出两种已批准用于治疗急性躁狂症的药物：奥氮平和喹硫平，它们具有抗抑郁活性，并且不会破坏情绪，因此是潜在的情绪稳定剂。本文旨在回顾有效治疗双相抑郁症的常规抗抑郁药和新型药物的作用机理。据推测，许多机制在双相抑郁症的有效治疗中发挥作用，包括5-羟色胺（5-HT），去甲肾上腺素，多巴胺，γ-氨基丁酸（GABA），谷氨酸和多种第二信使信号传导等靶标。途径。数据审查显示，抗抑郁药奥氮平和喹硫平具有重要的共性。抗抑郁药治疗（例如去甲肾上腺素再摄取抑制剂，SSRI和电惊厥疗法）会导致5-HT（2A）受体减少。奥氮平和喹硫平不仅是该受体的拮抗剂，而且还诱导5-HT（2A）受体的下调。这些药物的抗抑郁功效可能是由该受体介导的，而奥氮平和喹硫平在稳定情绪方面优于单峰抗抑郁治疗，其伴随的多巴胺D（2）拮抗作用可能会提供其他益处。应该进行进一步的研究以检验这些假设。

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