Expression of neuronal nicotinic acetylcholine receptors in rat vagal pulmonary sensory neurons

Qihai Gu; Dan Ni; Lu Yuan Lee

doi:10.1016/j.resp.2007.11.006

Expression of neuronal nicotinic acetylcholine receptors in rat vagal pulmonary sensory neurons

Qihai Gu, Dan Ni, Lu Yuan Lee

Physiology

Research output: Contribution to journal › Article › peer-review

25 Scopus citations

Abstract

It is known that cigarette smoke inhalation causes airway irritation and cough, and the effect is caused by both direct and indirect stimulatory effects of nicotine on bronchopulmonary sensory nerves. However, little is known about the expression of nicotinic acetylcholine receptors (nAChRs) in these afferents. In the present study, whole-cell patch-clamp recording and RT-PCR were carried out to examine the expression and function of nAChRs in isolated rat vagal pulmonary sensory neurons that were identified by retrograde labeling with a fluorescent tracer. Patch-clamp recordings demonstrated that application of acetylcholine concentration-dependently evoked an inward current in a subset of pulmonary sensory neurons, which was inhibited by hexamethonium. Application of nicotine or 1,1-dimethyl-4-phenylpiperazinium (DMPP) also activated these neurons, evoking an inward current in voltage-clamp configuration and causing depolarization and action potential in current-clamp recordings. RT-PCR analysis further demonstrated the expression of mRNA encoding for the nAChR subunits α4, α5, α6, α7, β2, β3 and β4, but not α2 and α3 in these neurons.

Original language	English
Pages (from-to)	87-91
Number of pages	5
Journal	Respiratory Physiology and Neurobiology
Volume	161
Issue number	1
DOIs	https://doi.org/10.1016/j.resp.2007.11.006
State	Published - Mar 20 2008

Bibliographical note

Funding Information:
We thank Guangfan Zhang, Michelle E. Wiggers and Ruei-Lung Lin for their technical assistance. This study was supported by grant HL067379 from the National Heart Lung and Blood Institute. Q. Gu is a Parker B. Francis Fellow in Pulmonary Research.

Funding

We thank Guangfan Zhang, Michelle E. Wiggers and Ruei-Lung Lin for their technical assistance. This study was supported by grant HL067379 from the National Heart Lung and Blood Institute. Q. Gu is a Parker B. Francis Fellow in Pulmonary Research.

Funders	Funder number
National Heart, Lung, and Blood Institute (NHLBI)	R01HL058686
National Heart and Lung Institute

Keywords

Airway irritation
Cough
Nicotinic acetylcholine receptor
Pulmonary sensory neuron

ASJC Scopus subject areas

General Neuroscience
Physiology
Pulmonary and Respiratory Medicine

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10.1016/j.resp.2007.11.006

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title = "Expression of neuronal nicotinic acetylcholine receptors in rat vagal pulmonary sensory neurons",

abstract = "It is known that cigarette smoke inhalation causes airway irritation and cough, and the effect is caused by both direct and indirect stimulatory effects of nicotine on bronchopulmonary sensory nerves. However, little is known about the expression of nicotinic acetylcholine receptors (nAChRs) in these afferents. In the present study, whole-cell patch-clamp recording and RT-PCR were carried out to examine the expression and function of nAChRs in isolated rat vagal pulmonary sensory neurons that were identified by retrograde labeling with a fluorescent tracer. Patch-clamp recordings demonstrated that application of acetylcholine concentration-dependently evoked an inward current in a subset of pulmonary sensory neurons, which was inhibited by hexamethonium. Application of nicotine or 1,1-dimethyl-4-phenylpiperazinium (DMPP) also activated these neurons, evoking an inward current in voltage-clamp configuration and causing depolarization and action potential in current-clamp recordings. RT-PCR analysis further demonstrated the expression of mRNA encoding for the nAChR subunits α4, α5, α6, α7, β2, β3 and β4, but not α2 and α3 in these neurons.",

keywords = "Airway irritation, Cough, Nicotinic acetylcholine receptor, Pulmonary sensory neuron",

author = "Qihai Gu and Dan Ni and Lee, {Lu Yuan}",

note = "Funding Information: We thank Guangfan Zhang, Michelle E. Wiggers and Ruei-Lung Lin for their technical assistance. This study was supported by grant HL067379 from the National Heart Lung and Blood Institute. Q. Gu is a Parker B. Francis Fellow in Pulmonary Research.",

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AU - Ni, Dan

AU - Lee, Lu Yuan

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N2 - It is known that cigarette smoke inhalation causes airway irritation and cough, and the effect is caused by both direct and indirect stimulatory effects of nicotine on bronchopulmonary sensory nerves. However, little is known about the expression of nicotinic acetylcholine receptors (nAChRs) in these afferents. In the present study, whole-cell patch-clamp recording and RT-PCR were carried out to examine the expression and function of nAChRs in isolated rat vagal pulmonary sensory neurons that were identified by retrograde labeling with a fluorescent tracer. Patch-clamp recordings demonstrated that application of acetylcholine concentration-dependently evoked an inward current in a subset of pulmonary sensory neurons, which was inhibited by hexamethonium. Application of nicotine or 1,1-dimethyl-4-phenylpiperazinium (DMPP) also activated these neurons, evoking an inward current in voltage-clamp configuration and causing depolarization and action potential in current-clamp recordings. RT-PCR analysis further demonstrated the expression of mRNA encoding for the nAChR subunits α4, α5, α6, α7, β2, β3 and β4, but not α2 and α3 in these neurons.

AB - It is known that cigarette smoke inhalation causes airway irritation and cough, and the effect is caused by both direct and indirect stimulatory effects of nicotine on bronchopulmonary sensory nerves. However, little is known about the expression of nicotinic acetylcholine receptors (nAChRs) in these afferents. In the present study, whole-cell patch-clamp recording and RT-PCR were carried out to examine the expression and function of nAChRs in isolated rat vagal pulmonary sensory neurons that were identified by retrograde labeling with a fluorescent tracer. Patch-clamp recordings demonstrated that application of acetylcholine concentration-dependently evoked an inward current in a subset of pulmonary sensory neurons, which was inhibited by hexamethonium. Application of nicotine or 1,1-dimethyl-4-phenylpiperazinium (DMPP) also activated these neurons, evoking an inward current in voltage-clamp configuration and causing depolarization and action potential in current-clamp recordings. RT-PCR analysis further demonstrated the expression of mRNA encoding for the nAChR subunits α4, α5, α6, α7, β2, β3 and β4, but not α2 and α3 in these neurons.

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Expression of neuronal nicotinic acetylcholine receptors in rat vagal pulmonary sensory neurons

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

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