ArticleNeuroscience2010
Inwardly rectifying potassium channel Kir4.1 is responsible for the native inward potassium conductance of satellite glial cells in sensory ganglia.
Article in Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 90 citations in OpenAlex.
- Lanthionine synthetase C-like protein 1 (LanCL1): a therapeutic target for neuropathic pain.Pain · 2026Article
- Aberrant astroglial Kir4.1 activation in the anterior cingulate cortex disrupts neuronal excitability and social behavior.Acta pharmaceutica Sinica. B · 2026Article
- Discovery of a Novel and Potent Kir4.1 Inhibitor as a Safe and Rapid-Onset Antidepressant Agent in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Retrograde control of sympathetic neuron-satellite glia interactions by target-derived NGF signaling.Cell reports · 2025Article
- Review
- Distinctive glial cells in the dorsal root ganglion: their morphology and functions.Anatomical science international · 2025Review
- Preclinical Insights into the Role of Kir4.1 in Chronic Pain and Depression: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- Distinct expression profile reveals glia involvement in the trigeminal system attributing to post-traumatic headache.The journal of headache and pain · 2024Article
- Article
- Satellite glial GPR37L1 and its ligand maresin 1 regulate potassium channel signaling and pain homeostasis.The Journal of clinical investigation · 2024Article
- Store-operated calcium entry in the satellite glial cells of rat sympathetic ganglia.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Characterisation of GFAP-Expressing Glial Cells in the Dorsal Root Ganglion after Spared Nerve Injury.International journal of molecular sciences · 2023Article
- One immune system plays many parts: The dynamic role of the immune system in chronic pain and opioid pharmacology.Neuropharmacology · 2023Review
- The Similar and Distinct Roles of Satellite Glial Cells and Spinal Astrocytes in Neuropathic Pain.Cells · 2023Review
- Review
- Article
- Peripheral mechanisms of chronic pain.Medical review (2021) · 2022Review
- Satellite Glial Cells: Morphology, functional heterogeneity, and role in pain.Frontiers in cellular neuroscience · 2022Review
- Comparative transcriptional analysis of satellite glial cell injury response.Wellcome open research · 2022Article
- Phenotypical changes of satellite glial cells in a murine model of GJournal of cellular and molecular medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Satellite glial cells (SGCs) surround primary afferent neurons in sensory ganglia, and increasing evidence has implicated the K(+) channels of SGCs in affecting or regulating sensory ganglion excitability. The inwardly rectifying K(+) (Kir) channel Kir4.1 is highly expressed in several types of glial cells in the central nervous system (CNS) where it has been implicated in extracellular K(+) concentration buffering. Upon neuronal activity, the extracellular K(+) concentration increases, and if not corrected, causes neuronal depolarization and uncontrolled changes in neuronal excitability. Recently, it has been demonstrated that knockdown of Kir4.1 expression in trigeminal ganglia leads to neuronal hyperexcitability in this ganglia and heightened nociception. Thus, we investigated the contribution of Kir4.1 to the membrane K(+) conductance of SGCs in neonatal and adult mouse trigeminal and dorsal root ganglia. Whole cell patch clamp recordings were performed in conjunction with immunocytochemistry and quantitative transcript analysis in various mouse lines. We found that in wild-type mice, the inward K(+) conductance of SGCs is blocked almost completely with extracellular barium, cesium and desipramine, consistent with a conductance mediated by Kir channels. We then utilized mouse lines in which genetic ablation led to partial or complete loss of Kir4.1 expression to assess the role of this channel subunit in SGCs. The inward K(+) currents of SGCs in Kir4.1+/- mice were decreased by about half while these currents were almost completely absent in Kir4.1-/- mice. These findings in combination with previous reports support the notion that Kir4.1 is the principal Kir channel type in SGCs. Therefore Kir4.1 emerges as a key regulator of SGC function and possibly neuronal excitability in sensory ganglia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.