ArticlePsychopharmacology2022
Antidepressant activity of pharmacological and genetic deactivation of the small-conductance calcium-activated potassium channel subtype-3.
Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Nitrous oxide activates layer 5 prefrontal neurons via SK2 channel inhibition for antidepressant effect.Nature communications · 2025Article
- Potassium channels in depression: emerging roles and potential targets.Cell & bioscience · 2024Review
- Article
- Chronic activation of the small-conductance, calcium-activated potassium channel precipitates age-dependent depressive-like behavior and cognitive deficits and reduces klotho concentration.Neuroscience applied · 2024Article
- Inhibition of SK Channels in VTA Affects Dopaminergic Neurons to Improve the Depression-Like Behaviors of Post-Stroke Depression Rats.Neuropsychiatric disease and treatment · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe voltage-insensitive, small-conductance calcium-activated potassium (SK) channel is a key regulator of neuronal depolarization and is implicated in the pathophysiology of depressive disorders.
objectiveWe ascertained whether the SK channel is impaired in the chronic unpredictable stress (CUS) model and whether it can serve as a molecular target of antidepressant action.
methodsWe assessed the depressive-like behavioral phenotype of CUS-exposed rats and performed post-mortem SK channel binding and activity-dependent zif268 mRNA analyses on their brains. To begin an assessment of SK channel subtypes involved, we examined the effects of genetic and pharmacological inhibition of the SK3 channel using conditional knockout mice and selective SK3 channel negative allosteric modulators (NAMs).
resultsWe found that [
conclusionsTaken together, these findings link depression-related neural and behavioral pathophysiology with abnormal SK channel functioning and suggest that this can be reversed by the selective inhibition of SK3 channels.
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Registered trials
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