K+ 通道与抑郁症的关系以及抗抑郁药对这些通道的药理作用。

IF 5.8 1区 医学 Q1 PSYCHIATRY Translational Psychiatry Pub Date : 2024-10-02 DOI:10.1038/s41398-024-03069-6
Xian-Tao Li
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引用次数: 0

摘要

抑郁症是一种常见而复杂的精神疾病,具有多种临床症状,甚至会导致残疾和自杀。由于对抑郁样障碍的发病机理认识不足,现有的药物治疗策略主要基于 "单胺类假说",结果在临床实践中疗效有限,并产生了许多不良反应。多重致病因素的概念有助于明确抑郁症的病因并开发抗抑郁药物。有资料表明,K+通道在调节大脑神经元兴奋性和神经递质释放方面起着至关重要的作用,这些通道的异常参与了癫痫发作和阿尔茨海默病(AD)等多种中枢神经系统(CNS)病症的致病过程。临床和前临床证据还表明,几种类型的 K+ 通道参与抑郁样行为似乎是显而易见的,这表明这些通道是导致这种衰弱性疾病的多种病因之一。新出现的数据表明,不同的抗抑郁药物会影响不同的 K+ 通道,如 Kv、Kir 和 K2P,这意味着这些药物通过 "多靶点 "方式发挥作用。另一方面,抗抑郁药影响 K+ 通道的情况可以为临床试验中的药理作用和众多副作用提供另一种解释。此外,这些通道可被视为 "可药物靶点",以开发新型治疗化合物来拮抗这种精神疾病。
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The involvement of K+ channels in depression and pharmacological effects of antidepressants on these channels.

Depression is a common and complex psychiatric illness with multiple clinical symptoms, even leading to the disability and suicide. Owing to the partial understanding of the pathogenesis of depressive-like disorders, available pharmacotherapeutic strategies are developed mainly based on the "monoamine hypothesis", resulting in a limited effectiveness and a number of adverse effects in the clinical practice. The concept of multiple pathogenic factors be helpful for clarifying the etiology of depression and developing the antidepressants. It is well documented that K+ channels serve crucial roles in modulating the neuronal excitability and neurotransmitter release in the brain, and abnormality of these channels participated in the pathogenic process of diverse central nervous system (CNS) pathologies, such as seizure and Alzheimer's disease (AD). The clinical and preclinical evidence also delineates that the involvement of several types of K+ channels in depressive-like behaviors appear to be evident, suggesting these channels being one of the multiple factors in the etiology of this debilitating disorder. Emerging data manifest that diverse antidepressants impact distinct K+ channels, such as Kv, Kir and K2P, meaning the functioning of these drug via a "multi-target" manner. On the other hand, the scenario of antidepressants impinging K+ channels could render an alternative interpretation for the pharmacological effectiveness and numerous side effects in clinical trials. Furthermore, these channels serve to be considered as a "druggable target" to develop novel therapeutic compound to antagonize this psychiatry.

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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
期刊最新文献
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