Secondhand smoke exposure alters K+ channel function and intrinsic cell excitability in a subset of second-order airway neurons in the nucleus tractus solitarius of young guinea pigs

Extended exposure to secondhand smoke (SHS) in infants and young children increases the incidence of cough, wheeze, airway hyper‐reactivity and the prevalence and earlier onset of asthma. The adverse effects may result from environmentally‐induced plasticity in the neural network regulating cough an...

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Bibliographic Details
Published in:The European journal of neuroscience 2010-02, Vol.31 (4), p.673-684
Main Authors: Sekizawa, Shin-ichi, Joad, Jesse P., Pinkerton, Kent E., Bonham, Ann C.
Format: Article
Language:English
Subjects:
4-Aminopyridine - pharmacology
Action Potentials - drug effects
airway afferent fibers
Animals
environmental air pollutants
Guinea Pigs
In Vitro Techniques
intrinsic cell excitability
ion channels
K+ currents
Lung - innervation
Male
Membrane Potentials - drug effects
Neuroanatomical Tract-Tracing Techniques
Neurons, Afferent - metabolism
Neurons, Afferent - physiology
postsynaptic neurons
Potassium Channel Blockers - pharmacology
Random Allocation
Solitary Nucleus - drug effects
Solitary Nucleus - metabolism
Solitary Nucleus - physiology
Tetraethylammonium - pharmacology
Tobacco Smoke Pollution - adverse effects
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Summary:Extended exposure to secondhand smoke (SHS) in infants and young children increases the incidence of cough, wheeze, airway hyper‐reactivity and the prevalence and earlier onset of asthma. The adverse effects may result from environmentally‐induced plasticity in the neural network regulating cough and airway function. Using whole‐cell patch‐clamp recordings in brainstem slices containing anatomically identified second‐order lung afferent neurons in the nucleus tractus solitarius (NTS), we determined the effects of extended SHS exposure in young guinea pigs for a duration equivalent to human childhood on the intrinsic excitability of NTS neurons. SHS exposure resulted in marked decreases in the intrinsic excitability of a subset of lung afferent second‐order NTS neurons. The neurons exhibited a decreased spiking capacity, prolonged action potential duration, reduced afterhyperpolarization, decrease in peak and steady‐state outward currents, and membrane depolarization. SHS exposure effects were mimicked by low concentrations of the K+ channel blockers 4‐aminopyridine and/or tetraethyl ammonium. The data suggest that SHS exposure downregulates K+ channel function in a subset of NTS neurons, resulting in reduced cell excitability. The changes may help to explain the exaggerated neural reflex responses in children exposed to SHS.
ISSN:0953-816X
1460-9568
DOI:10.1111/j.1460-9568.2010.07093.x