KCNS1

Last update 08 May 2025

Basic Info

Synonyms

Delayed-rectifier K(+) channel alpha subunit 1, KCNS1, Kv9.1

+ [5]

Introduction

Potassium channel regulatory subunit that modulate the delayed rectifier voltage-gated potassium channel activity of KCNB1 and KCNB2 by altering their kinetics, expression levels, and shifting the half-inactivation potential to more polarized values (PubMed:10484328). While it does not form functional channels on its own, it can form functional heterotetrameric channels with KCNB1 and KCNB2 (PubMed:10484328). Each regulatory subunit has unique regulatory properties that can lead to extensive inhibition, significant changes in kinetics, and/or substantial shifts in the voltage dependencies of the inactivation process (By similarity).

100 Clinical Results associated with KCNS1

100 Translational Medicine associated with KCNS1

0 Patents (Medical) associated with KCNS1

Literatures (Medical) associated with KCNS1

01 May 2025·Anesthesia & Analgesia

mRNA Expression of Mineralocorticoid and Glucocorticoid Receptors in Human and Mouse Sensory Neurons of the Dorsal Root Ganglia

Article

Author: Zhang, Jun-Ming ; Kadakia, Feni K. ; Serafin, Elizabeth K. ; Qualls, Katherine A. ; Lückemeyer, Debora De Nardin ; Strong, Judith A. ; Davidson, Steve

BACKGROUND:Corticosteroid receptors, including mineralocorticoid receptor (MR) and glucocorticoid receptor (GR), play important roles in inflammatory pain in the dorsal root ganglion (DRG). Although it is widely known that activating the GR reduces inflammatory pain, it has recently been shown that MR activation contributes to pain and neuronal excitability in rodent studies. Moreover, little is known about the translation of this work to humans, or the mechanisms through which corticosteroid receptors regulate inflammatory pain.METHODS:Corticosteroid receptor expression in human and mouse DRGs was characterized. RNAscope was used to perform high-resolution in situ hybridization for GR and MR mRNAs and to examine their colocalization with markers for nociceptors (SCN10A, NaV1.8 mRNA) and Aβ mechanoreceptors (KCNS1, Kv9.1 mRNA) in human DRG and C57BL/6J mouse DRG samples.RESULTS:GR and MR mRNAs are expressed in almost all DRG neurons across species. The 2 receptors colocalize in 99.2% of human DRG neurons and 95.9% of mouse DRG neurons (P = .0004, Fisher exact test). In both human and mouse DRGs, the large-diameter KCNS1+ Aβ mechanoreceptors showed a significantly higher MR/GR ratio (MR-leaning) compared to KCNS1− neurons (human: 0.23 vs 0.04, P = .0002; mouse: 0.35 vs −0.24, P < .0001; log ratios, unpaired t test), whereas small-diameter SCN10A+ nociceptive neurons showed a significantly lower MR/GR ratio (GR-leaning) compared to SCN10A− neurons (human: −0.02 vs 0.18, P = .0001; mouse: −0.16 vs 0.08, P < .0001; log ratios, unpaired t test).CONCLUSIONS:These findings indicate that mouse corticosteroid receptor mRNA expression reflects human expression in the DRG, and that mice could be a suitable model for studying corticosteroid receptor involvement in pain. Additionally, this study supports the translatability of rodent data to humans for the use of more selective corticosteroids at the DRG in pain treatments.

01 Dec 2023·Naunyn-Schmiedeberg's Archives of Pharmacology

Parthenolide as a potential analgesic in the treatment of paclitaxel-induced neuropathic pain: the rat modeling

Article

Author: Bayram, Cemil ; Budak, Harun ; Özkaraca, Mustafa ; Sezen, Selma ; Hacımüftüoğlu, Ahmet ; Toraman, Emine

In this study, we determined the therapeutic effect of parthenolide (PTL), the active component of Tanacetum parthenium, on neuropathic pain caused by paclitaxel (PTX), a chemotherapeutic drug frequently used in cancer treatment, at the gene and protein levels. To this end, 6 groups were formed: control, PTX, sham, 1 mg/PTL, 2 mg/kg PTL, and 4 mg/kg PTL. Pain formation was tested by Randall-Selitto analgesiometry and locomotor activity behavioral analysis. Then, PTL treatment was performed for 14 days. After the last dose of PTL was taken, Hcn2, Trpa1, Scn9a, and Kcns1 gene expressions were measured in rat brain (cerebral cortex/CTX) tissues. In addition, changes in the levels of SCN9A and KCNS1 proteins were determined by immunohistochemical analysis. Histopathological hematoxylin-eosin staining was also performed to investigate the effect of PTL in treating tissue damage on neuropathic pain caused by PTX treatment. When the obtained data were analyzed, pain threshold and locomotor activity decreased in PTX and sham groups and increased with PTL treatment. In addition, it was observed that the expression of the Hcn2, Trpa1, and Scn9a genes decreased while the Kcns1 gene expression increased. When protein levels were examined, it was determined that SCN9A protein expression decreased and the KCNS1 protein level increased. It was determined that PTL treatment also improved PTX-induced tissue damage. The results of this study demonstrate that non-opioid PTL is an effective therapeutic agent in the treatment of chemotherapy-induced neuropathic pain, especially when used at a dose of 4 mg/kg acting on sodium and potassium channels.

01 Feb 2023·Molecular Psychiatry

Cortical profiles of numerous psychiatric disorders and normal development share a common pattern

Article

Author: Brühl, Rüdiger ; Conrod, Patricia ; Walter, Henrik ; Hohmann, Sarah ; Schwab, Nathan ; Millenet, Sabina ; Veltman, Dick J ; Sinha, Rajita ; Zhu, Alyssa ; Poustka, Luise ; Thompson, Paul M ; van Holst, Ruth J ; Schmaal, Lianne ; Gowland, Penny ; Orfanos, Dimitri Papadopoulos ; Lett, Tristram ; Cao, Zhipeng ; Goudriaan, Anna E ; Wiers, Reinout W ; Porjesz, Bernice ; Winterer, Jeanne ; Chaarani, Bader ; Albaugh, Matthew ; Murphy, Alistair ; Robinson, Lauren ; Whelan, Robert ; Groefsema, Martine ; Artiges, Eric ; Mackey, Scott ; Cupertino, Renata B ; Flor, Herta ; Bhatt, Ravi R ; Juliano, Anthony ; Nees, Frauke ; Pancholi, Devarshi ; Yuan, Dekang ; Grigis, Antoine ; Jahanshad, Neda ; Garavan, Hugh ; Stafford, James ; Hutchison, Kent ; Heinz, Andreas ; Momenan, Reza ; Li, Chiang-Shan R ; Banaschewski, Tobias ; Fröhner, Juliane H ; Desrivières, Sylvane ; Martinot, Marie-Laure Paillère ; Luijten, Maartje ; Paus, Tomáš ; Ottino-Gonzalez, Jonatan ; Schumann, Gunter ; Smolka, Michael N ; Martinot, Jean-Luc ; Bokde, Arun L W

The neurobiological bases of the association between development and psychopathology remain poorly understood. Here, we identify a shared spatial pattern of cortical thickness (CT) in normative development and several psychiatric and neurological disorders. Principal component analysis (PCA) was applied to CT of 68 regions in the Desikan-Killiany atlas derived from three large-scale datasets comprising a total of 41,075 neurotypical participants. PCA produced a spatially broad first principal component (PC1) that was reproducible across datasets. Then PC1 derived from healthy adult participants was compared to the pattern of CT differences associated with psychiatric and neurological disorders comprising a total of 14,886 cases and 20,962 controls from seven ENIGMA disease-related working groups, normative maturation and aging comprising a total of 17,697 scans from the ABCD Study® and the IMAGEN developmental study, and 17,075 participants from the ENIGMA Lifespan working group, as well as gene expression maps from the Allen Human Brain Atlas. Results revealed substantial spatial correspondences between PC1 and widespread lower CT observed in numerous psychiatric disorders. Moreover, the PC1 pattern was also correlated with the spatial pattern of normative maturation and aging. The transcriptional analysis identified a set of genes including KCNA2, KCNS1 and KCNS2 with expression patterns closely related to the spatial pattern of PC1. The gene category enrichment analysis indicated that the transcriptional correlations of PC1 were enriched to multiple gene ontology categories and were specifically over-represented starting at late childhood, coinciding with the onset of significant cortical maturation and emergence of psychopathology during the prepubertal-to-pubertal transition. Collectively, the present study reports a reproducible latent pattern of CT that captures interregional profiles of cortical changes in both normative brain maturation and a spectrum of psychiatric disorders. The pubertal timing of the expression of PC1-related genes implicates disrupted neurodevelopment in the pathogenesis of the spectrum of psychiatric diseases emerging during adolescence.

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