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Updated: Aug 7, 2026

A Method of Nodose Ganglia Injection in Sprague-Dawley Rat
Published on: November 25, 2014
A neuroactive steroid inhibits guinea pig airway sensory nerves via Maxi-K channel activation
Shigemi Yoshihara1, Hiroshi Morimoto, Makoto Ohori
1Department of Pediatrics, Dokkyo University School of Medicine, Tochigi, Japan. shigemi@dokkyomed.ac.jp
Background:
Although neurogenic inflammation via the activation of C-fibers in the airway may have an important role in the pathogenesis of asthma, their regulatory mechanism remains uncertain.
Objective:
The pharmacological profiles of a neuroactive steroid, allotetrahydrocorticosterone, on the activation of C-fibers in airway tissues were investigated, and the mechanism how a neuroactive steroid regulates airway inflammatory reactions was clarified.
Methods:
The effects of allotetrahydrocorticosterone on electrical field stimulation-induced bronchial smooth muscle contraction in guinea pig airway tissues were investigated. The influences of K+ channel blockers and intracellular protein inhibitors on the effects of allotetrahydrocorticosterone were examined.
Results:
Allotetrahydrocorticosterone dose-dependently inhibited electrical field stimulation-induced guinea pig bronchial smooth muscle contraction. The inhibitory effects of allotetrahydrocorticosterone on electrical field stimulation-induced bronchial contraction were reduced by the pretreatment of Maxi-K+ channel blockers, iberiotoxin and charybdotoxin, but not other K+ channel blockers, dendrotoxin or glibenclamide. Pretreatment with pertussis toxin diminished the inhibitory effect of allotetrahydrocorticosterone, but not an adenylate cyclase inhibitor, SQ 22536, nor a specific inhibitor of mitogen-activated protein kinase kinase, PD 98059.
Conclusions:
These findings suggest that allotetrahydrocorticosterone negatively modulates the activation of C-fibers in guinea pig airway tissues via the opening of Maxi-K+ channels and a pertussis toxin-sensitive G-protein-coupled mechanism.
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