ArticlePloS one2009
Predominant functional expression of Kv1.3 by activated microglia of the hippocampus after Status epilepticus.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- Non-conducting functions of potassium channels in cancer and neurological disease.Current topics in membranes · 2023Review
- Microglial diversity along the hippocampal longitudinal axis impacts synaptic plasticity in adult male mice under homeostatic conditions.Journal of neuroinflammation · 2022Article
- Microglial ion channels: Key players in non-cell autonomous neurodegeneration.Neurobiology of disease · 2022Review
- Revealing the Precise Role of Calretinin Neurons in Epilepsy: We Are on the Way.Neuroscience bulletin · 2022Review
- Microglial Potassium Channels: From Homeostasis to Neurodegeneration.Biomolecules · 2021Review
- Treatment of Radiation-Induced Brain Necrosis.Oxidative medicine and cellular longevity · 2021Review
- Review on Biological Characteristics of Kv1.3 and Its Role in Liver Diseases.Frontiers in pharmacology · 2021Review
- Article
- Microglia in Alzheimer's Disease: A Role for Ion Channels.Frontiers in neuroscience · 2018Review
- Sex- and Development-Dependent Responses of Rat Microglia to Pro- and Anti-inflammatory Stimulation.Frontiers in cellular neuroscience · 2018Article
- Responses of rat and mouse primary microglia to pro- and anti-inflammatory stimuli: molecular profiles, KJournal of neuroinflammation · 2017Article
- Potassium channel expression and function in microglia: Plasticity and possible species variations.Channels (Austin, Tex.) · 2017Review
- A systems pharmacology-based approach to identify novel Kv1.3 channel-dependent mechanisms in microglial activation.Journal of neuroinflammation · 2017Article
- Margatoxin-bound quantum dots as a novel inhibitor of the voltage-gated ion channel Kv1.3.Journal of neurochemistry · 2017Article
- Targeting Kv1.3 channels to reduce white matter pathology after traumatic brain injury.Experimental neurology · 2016Article
- KV1 and KV3 Potassium Channels Identified at Presynaptic Terminals of the Corticostriatal Synapses in Rat.Neural plasticity · 2016Article
- Article
- Potassium channel Kv1.3 is highly expressed by microglia in human Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2015Article
- Defective microglial development in the hippocampus of Cx3cr1 deficient mice.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGrowing evidence indicates that the functional state of microglial cells differs according to the pathological conditions that trigger their activation. In particular, activated microglial cells can express sets of Kv subunits which sustain delayed rectifying potassium currents (Kdr) and modulate differently microglia proliferation and ability to release mediators. We recently reported that hippocampal microglia is in a particular activation state after a status epilepticus (SE) and the present study aimed at identifying which of the Kv channels are functionally expressed by microglia in this model. METHODOLOGY/PRINCIPAL
findingsSE was induced by systemic injection of kainate in CX3CR1(eGFP/+) mice and whole cell recordings of fluorescent microglia were performed in acute hippocampal slices prepared 48 h after SE. Microglia expressed Kdr currents which were characterized by a potential of half-maximal activation near -25 mV, prominent steady-state and cumulative inactivations. Kdr currents were almost abolished by the broad spectrum antagonist 4-Aminopyridine (1 mM). In contrast, tetraethylammonium (TEA) at a concentration of 1 mM, known to block Kv3.1, Kv1.1 and 1.2 subunits, only weakly reduced Kdr currents. However, at a concentration of 5 mM which should also affect Kv1.3 and 1.6, TEA inhibited about 30% of the Kdr conductance. Alpha-dendrotoxin, which selectively inhibits Kv1.1, 1.2 and 1.6, reduced only weakly Kdr currents, indicating that channels formed by homomeric assemblies of these subunits are not important contributors of Kdr currents. Finally, agitoxin-2 and margatoxin strongly inhibited the current. CONCLUSIONS/SIGNIFICANCE: These results indicate that Kv1.3 containing channels predominantly determined Kdr currents in activated microglia after SE.
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