Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour

Two pore domain potassium (K2P) channels (KCNKx.x) cause K + leak currents and are major contributors to resting membrane potential. Their roles in dorsal root ganglion (DRG) neurons normally, and in pathological pain models, are poorly understood. Therefore, we examined mRNA levels for 10 K2P chann...

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Main Authors: Marsh, Barnaby, Acosta, Cristian, Djouhri, Laiche, Lawson, Sally N.
Format: Online
Language:English
Published: Academic Press 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3334831/
id pubmed-3334831
recordtype oai_dc
spelling pubmed-33348312012-04-26 Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour Marsh, Barnaby Acosta, Cristian Djouhri, Laiche Lawson, Sally N. Article Two pore domain potassium (K2P) channels (KCNKx.x) cause K + leak currents and are major contributors to resting membrane potential. Their roles in dorsal root ganglion (DRG) neurons normally, and in pathological pain models, are poorly understood. Therefore, we examined mRNA levels for 10 K2P channels in L4 and L5 rat DRGs normally, and 1 day and 4 days after unilateral cutaneous inflammation, induced by intradermal complete Freund's adjuvant (CFA) injections. Spontaneous foot lifting (SFL) duration (spontaneous pain behaviour) was measured in 1 day and 4 day rats < 1 h before DRG harvest. mRNA levels for KCNK channels and Kv1.4 relative to GAPDH (n = 4–6 rats/group) were determined with real-time RT-PCR. This study is the first to demonstrate expression of THIK1, THIK2 and TWIK2 mRNA in DRGs. Abundance in normal DRGs was, in descending order: Academic Press 2012-03 /pmc/articles/PMC3334831/ /pubmed/22273507 http://dx.doi.org/10.1016/j.mcn.2012.01.002 Text en © 2012 Elsevier Inc. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Marsh, Barnaby
Acosta, Cristian
Djouhri, Laiche
Lawson, Sally N.
spellingShingle Marsh, Barnaby
Acosta, Cristian
Djouhri, Laiche
Lawson, Sally N.
Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour
author_facet Marsh, Barnaby
Acosta, Cristian
Djouhri, Laiche
Lawson, Sally N.
author_sort Marsh, Barnaby
title Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour
title_short Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour
title_full Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour
title_fullStr Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour
title_full_unstemmed Leak K+ channel mRNAs in dorsal root ganglia: Relation to inflammation and spontaneous pain behaviour
title_sort leak k+ channel mrnas in dorsal root ganglia: relation to inflammation and spontaneous pain behaviour
description Two pore domain potassium (K2P) channels (KCNKx.x) cause K + leak currents and are major contributors to resting membrane potential. Their roles in dorsal root ganglion (DRG) neurons normally, and in pathological pain models, are poorly understood. Therefore, we examined mRNA levels for 10 K2P channels in L4 and L5 rat DRGs normally, and 1 day and 4 days after unilateral cutaneous inflammation, induced by intradermal complete Freund's adjuvant (CFA) injections. Spontaneous foot lifting (SFL) duration (spontaneous pain behaviour) was measured in 1 day and 4 day rats < 1 h before DRG harvest. mRNA levels for KCNK channels and Kv1.4 relative to GAPDH (n = 4–6 rats/group) were determined with real-time RT-PCR. This study is the first to demonstrate expression of THIK1, THIK2 and TWIK2 mRNA in DRGs. Abundance in normal DRGs was, in descending order:
publisher Academic Press
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3334831/
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