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氯胺酮:抑郁症中的神经生物学和生物分子探索。

Ketamine a dissociative anesthetic: Neurobiology and biomolecular exploration in depression.

机构信息

Department of Anesthesiology, The Second Hospital of Jilin University, Changchun, Jilin, China.

Department of Anesthesiology, The Second Hospital of Jilin University, Changchun, Jilin, China.

出版信息

Chem Biol Interact. 2020 Mar 1;319:109006. doi: 10.1016/j.cbi.2020.109006. Epub 2020 Feb 19.

DOI:10.1016/j.cbi.2020.109006
PMID:32084352
Abstract

Ketamine is gaining ground as a potential treating depression because it has a distinct mode of action than typical drugs that influence monoamine neurotransmitters including noradrenaline, dopamine, or serotonin. Ketamine is thought to act by blocking N-methyl-d-aspartate (NMDA) receptors in the brain, which interact with the amino acid neurotransmitter glutamate. The resultant chemical changes in the brain caused by ketamine are not yet fully understood but could involve ketamine-induced gene expression and signaling cascades that act long after the drug has been eliminated from the body. Despite these remarkable effects, the widespread use of ketamine is limited by potential side effects including the emergence reactions (hallucinations, dreams, and out-of-body experiences) by recreational users, who need further study before long-term use of ketamine can be approved for depression. Thus, studies are necessary to further elucidate mechanistic actions of ketamine at cellular and network levels. Thus, we are exploring the involvement of molecular targets for the treatment and psychomimetic phenomena of the ketamine.

摘要

氯胺酮作为一种有潜力的抗抑郁药物正在逐渐受到关注,因为它的作用模式与影响单胺神经递质(包括去甲肾上腺素、多巴胺或血清素)的典型药物不同。氯胺酮被认为通过阻断大脑中的 N-甲基-D-天冬氨酸(NMDA)受体起作用,NMDA 受体与氨基酸神经递质谷氨酸相互作用。氯胺酮在大脑中引起的化学变化尚未完全理解,但可能涉及氯胺酮诱导的基因表达和信号级联反应,这些反应在药物从体内消除后很长时间内仍然存在。尽管有这些显著的效果,但氯胺酮的广泛应用受到潜在副作用的限制,包括娱乐性使用者出现的反应(幻觉、梦境和离体体验),在长期使用氯胺酮治疗抑郁症之前,还需要进一步研究。因此,有必要进行研究以进一步阐明氯胺酮在细胞和网络水平上的作用机制。因此,我们正在探索氯胺酮的分子靶点在治疗和精神拟态现象中的作用。

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