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.
|Number of pages||5|
|Journal||Respiratory Physiology and Neurobiology|
|State||Published - Mar 20 2008|
Bibliographical noteFunding 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.
- Airway irritation
- Nicotinic acetylcholine receptor
- Pulmonary sensory neuron
ASJC Scopus subject areas
- Neuroscience (all)
- Pulmonary and Respiratory Medicine