ArticleFrontiers in molecular neuroscience2019
Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior.
Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 34 citations in OpenAlex.
- Sex-specific interneuron vulnerability after traumatic brain injury correlates with neurotrophic signaling and chloride homeostasis, independent of behavioral and network outcomes.Frontiers in cellular neuroscience · 2025Article
- Ectopic expression of the cation-chloride cotransporter KCC2 in blood exosomes as a biomarker for functional rehabilitation.Frontiers in molecular neuroscience · 2025Article
- Heterogeneous subpopulations of GABAiScience · 2024Article
- Article
- Bumetanide induces post-traumatic microglia-interneuron contact to promote neurogenesis and recovery.Brain : a journal of neurology · 2023Article
- Experimental and real-world evidence supporting the computational repurposing of bumetanide forNature aging · 2021Article
- Is High-Intensity Interval Training Suitable to Promote Neuroplasticity and Cognitive Functions after Stroke?International journal of molecular sciences · 2021Review
- Protective Role of Low Ethanol Administration Following Ischemic Stroke via Recovery of KCC2 and p75Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression, and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels are not available. Using controlled-cortical impact as an experimental model of brain trauma in adult mice, we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on the appearance of depressive-like behavior. We demonstrate that this alteration in behavior is associated with an impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in the expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission from hyperpolarizing to depolarizing after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.
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