Department of Molecular Neurochemistry, Faculty of Health Sciences, Medical University of Lodz, 92215 Lodz, Poland.
Int J Mol Sci. 2020 Nov 9;21(21):8410. doi: 10.3390/ijms21218410.
Ketamine is a non-competitive antagonist of NMDA (N-methyl-D-aspartate) receptor, which has been in clinical practice for over a half century. Despite recent data suggesting its harmful side effects, such as neuronal loss, synapse dysfunction or disturbed neural network formation, the drug is still applied in veterinary medicine and specialist anesthesia. Several lines of evidence indicate that structural and functional abnormalities in the nervous system caused by ketamine are crosslinked with the imbalanced activity of multiple Ca-regulated signaling pathways. Due to its ubiquitous nature, Ca is also frequently located in the center of ketamine action, although the precise mechanisms underlying drug's negative or therapeutic properties remain mysterious for the large part. This review seeks to delineate the relationship between ketamine-triggered imbalance in Ca homeostasis and functional consequences for downstream processes regulating key aspects of neuronal function.
氯胺酮是一种非竞争性 NMDA（N-甲基-D-天冬氨酸）受体拮抗剂，已经在临床实践中应用了半个多世纪。尽管最近有数据表明它有神经细胞丢失、突触功能障碍或神经网络形成障碍等有害的副作用，但该药物仍在兽医和专业麻醉中使用。有几条证据表明，氯胺酮引起的神经系统结构和功能异常与多个钙调节信号通路的失衡活动有关。由于钙的普遍性，它也经常位于氯胺酮作用的中心，尽管药物的负面或治疗特性的确切机制在很大程度上仍然是神秘的。这篇综述旨在描绘氯胺酮引起的钙稳态失衡与下游调节神经元功能关键方面的过程之间的关系。
