ArticlePain reports2026
Two pore domain THIK2 potassium channels regulate acute and chronic pain signaling.
Article in Pain reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- K2P channels as emerging therapeutic targets for pain: insights from functional studies and transcriptomic analyses.Frontiers in pharmacology · 2026Review
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11 authors.
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Abstract
Introduction: Two-pore domain potassium channels regulate neuronal excitability by generating background potassium currents that stabilize the resting membrane potential. Although several two-pore domain potassium channels have been implicated in pain signaling, the physiological role of tandem pore domain halotane-inhibited K+ channel (THIK2) remains largely unknown despite its high expression in human and mouse nociceptive dorsal root ganglion (DRG) neurons. Objective: This study aimed to determine the cellular distribution of THIK2 in sensory neurons and to investigate its contribution to neuronal excitability and nociceptive processing under physiological and inflammatory conditions. Methods: We combined molecular analyses, electrophysiological recordings, and behavioral approaches. THIK1 and THIK2 expression patterns were mapped in mouse DRGs. Whole-cell electrophysiology was used to assess membrane excitability in sensory neurons from wild-type and THIK2 Results: We provide the first comprehensive characterization of THIK1 and THIK2 expression in mouse DRG. THIK2 deletion increased neuronal firing during sustained stimulation, indicating a loss of tonic inhibitory control of membrane excitability, particularly in nonpeptidergic IB4-positive C-fiber neurons. Behaviorally, THIK2 Conclusion: THIK2 channels act as key regulators preventing pathological hyperexcitability in nociceptive sensory neurons. Their loss leads to increased neuronal firing and enhanced thermal sensitivity, identifying THIK2 as a promising therapeutic target for chronic inflammatory pain.
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