In physiological conditions, adult neurons have low intracellular Cl- [(Cl-)I] levels underlying the γ-aminobutyric acid (GABA)ergic inhibitory drive. In contrast, neurons have high (Cl-)I levels and excitatory GABA actions in a wide range of pathological conditions including spinal cord lesions, chronic pain, brain trauma, cerebrovascular infarcts, autism, Rett and Down syndrome, various types of epilepsies, and other genetic or environmental insults. The diuretic highly specific NKCC1 chloride importer antagonist bumetanide (PubChem CID: 2461) efficiently restores low (Cl-)I levels and attenuates many disorders in experimental conditions and in some clinical trials. Here, I review the mechanisms of action, therapeutic effects, promises, and pitfalls of bumetanide.

中文翻译：

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NKCC1 氯化物进口拮抗剂可减轻许多神经和精神疾病

在生理条件下，成年神经元的细胞内 Cl-[(Cl-)I] 水平较低，这是 γ-氨基丁酸 (GABA) 能抑制驱动的基础。相比之下，神经元在广泛的病理条件下具有高 (Cl-)I 水平和兴奋性 GABA 作用，包括脊髓损伤、慢性疼痛、脑外伤、脑血管梗塞、自闭症、Rett 和唐氏综合征、各种类型的癫痫和其他遗传或环境侮辱。利尿剂高特异性 NKCC1 氯化物导入拮抗剂布美他尼 (PubChem CID: 2461) 可有效恢复低 (Cl-)I 水平并减轻实验条件和一些临床试验中的许多疾病。在这里，我回顾了布美他尼的作用机制、治疗效果、前景和陷阱。