Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons

<p>Abstract</p> <p>Voltage-gated sodium channels (VGSCs) play an important role in the control of membrane excitability. We previously reported that the excitability of nociceptor was increased by hypotonic stimulation. The present study tested the effect of hypotonicity on tetrodo...

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Main Authors: Chen Lei, Liu Changjin, Li Lin, Chen Ling
Format: Article
Language:English
Published: SAGE Publishing 2011-04-01
Series:Molecular Pain
Subjects:
Online Access:http://www.molecularpain.com/content/7/1/27
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spelling doaj-a49af1f9078b4af5873fa1381659b9ee2020-11-25T03:07:31ZengSAGE PublishingMolecular Pain1744-80692011-04-01712710.1186/1744-8069-7-27Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neuronsChen LeiLiu ChangjinLi LinChen Ling<p>Abstract</p> <p>Voltage-gated sodium channels (VGSCs) play an important role in the control of membrane excitability. We previously reported that the excitability of nociceptor was increased by hypotonic stimulation. The present study tested the effect of hypotonicity on tetrodotoxin-sensitive sodium current (TTX-S current) in cultured trigeminal ganglion (TG) neurons. Our data show that after hypotonic treatment, TTX-S current was increased. In the presence of hypotonicity, voltage-dependent activation curve shifted to the hyperpolarizing direction, while the voltage-dependent inactivation curve was not affected. Transient Receptor Potential Vanilloid 4 receptor (TRPV4) activator increased TTX-S current and hypotonicity-induced increase was markedly attenuated by TRPV4 receptor blockers. We also demonstrate that inhibition of PKC attenuated hypotonicity-induced inhibition, whereas PKA system was not involved in hypotonic-response. We conclude that hypotonic stimulation enhances TTX-S current, which contributes to hypotonicity-induced nociception. TRPV4 receptor and PKC intracellular pathway are involved in the increase of TTX-S current by hypotonicity.</p> http://www.molecularpain.com/content/7/1/27hypotonicitytetrodotoxin-sensitive sodium currentTRPV4 receptorintracellular signaling pathwaynociception
collection DOAJ
language English
format Article
sources DOAJ
author Chen Lei
Liu Changjin
Li Lin
Chen Ling
spellingShingle Chen Lei
Liu Changjin
Li Lin
Chen Ling
Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons
Molecular Pain
hypotonicity
tetrodotoxin-sensitive sodium current
TRPV4 receptor
intracellular signaling pathway
nociception
author_facet Chen Lei
Liu Changjin
Li Lin
Chen Ling
author_sort Chen Lei
title Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons
title_short Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons
title_full Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons
title_fullStr Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons
title_full_unstemmed Hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons
title_sort hypotonicity modulates tetrodotoxin-sensitive sodium current in trigeminal ganglion neurons
publisher SAGE Publishing
series Molecular Pain
issn 1744-8069
publishDate 2011-04-01
description <p>Abstract</p> <p>Voltage-gated sodium channels (VGSCs) play an important role in the control of membrane excitability. We previously reported that the excitability of nociceptor was increased by hypotonic stimulation. The present study tested the effect of hypotonicity on tetrodotoxin-sensitive sodium current (TTX-S current) in cultured trigeminal ganglion (TG) neurons. Our data show that after hypotonic treatment, TTX-S current was increased. In the presence of hypotonicity, voltage-dependent activation curve shifted to the hyperpolarizing direction, while the voltage-dependent inactivation curve was not affected. Transient Receptor Potential Vanilloid 4 receptor (TRPV4) activator increased TTX-S current and hypotonicity-induced increase was markedly attenuated by TRPV4 receptor blockers. We also demonstrate that inhibition of PKC attenuated hypotonicity-induced inhibition, whereas PKA system was not involved in hypotonic-response. We conclude that hypotonic stimulation enhances TTX-S current, which contributes to hypotonicity-induced nociception. TRPV4 receptor and PKC intracellular pathway are involved in the increase of TTX-S current by hypotonicity.</p>
topic hypotonicity
tetrodotoxin-sensitive sodium current
TRPV4 receptor
intracellular signaling pathway
nociception
url http://www.molecularpain.com/content/7/1/27
work_keys_str_mv AT chenlei hypotonicitymodulatestetrodotoxinsensitivesodiumcurrentintrigeminalganglionneurons
AT liuchangjin hypotonicitymodulatestetrodotoxinsensitivesodiumcurrentintrigeminalganglionneurons
AT lilin hypotonicitymodulatestetrodotoxinsensitivesodiumcurrentintrigeminalganglionneurons
AT chenling hypotonicitymodulatestetrodotoxinsensitivesodiumcurrentintrigeminalganglionneurons
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