ArticlePhysiological reports2018
Potassium channels contribute to activity-dependent regulation of dendritic inhibition.
Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Transcranial High-Frequency Terahertz Stimulation Alleviates Anxiety-like Behavior in Mice via a Noninvasive Approach.Research (Washington, D.C.) · 2025Article
- Regulation of Rostral Nucleus of the Solitary Tract Responses to Afferent Input by A-type K+ Current.Neuroscience · 2022Article
- Potassium channels contribute to activity-dependent regulation of dendritic inhibition.Physiological reports · 2018Article
- Symbiotic Supplementation (Cell transplantationArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
GABAergic inhibition plays a critical role in the regulation of neuronal activity. In the neocortex, inhibitory interneurons that target the dendrites of pyramidal cells influence both electrical and biochemical postsynaptic signaling. Voltage-gated ion channels strongly shape dendritic excitability and the integration of excitatory inputs, but their contribution to GABAergic signaling is less well understood. By combining 2-photon calcium imaging and focal GABA uncaging, we show that voltage-gated potassium channels normally suppress the GABAergic inhibition of calcium signals evoked by back-propagating action potentials in dendritic spines and shafts of cortical pyramidal neurons. Moreover, the voltage-dependent inactivation of these channels leads to enhancement of dendritic calcium inhibition following somatic spiking. Computational modeling reveals that the enhancement of calcium inhibition involves an increase in action potential depolarization coupled with the nonlinear relationship between membrane voltage and calcium channel activation. Overall, our findings highlight the interaction between intrinsic and synaptic properties and reveal a novel mechanism for the activity-dependent regulation of GABAergic inhibition.
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Registered trials
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