Research

TRPM8 mechanism of autonomic nerve response to cold in respiratory airway

Hong Xing¹ , Jennifer X Ling¹ , Meng Chen¹ , Richard D Johnson² , Makoto Tominaga³ , Cong-Yi Wang⁴ and Jianguo Gu¹

¹  Department of Oral & Maxillofacial Surgery and Diagnostic Sciences, McKnight Brain Institute and College of Dentistry, University of Florida, Gainesville, Florida 32610, USA

²  Department of Physiological Sciences, McKnight Brain Institute and College of Veterinary Medicine, University of Florida, Gainesville, Florida 32610, USA

³  Section of Cell Signaling, Okazaki Institute for Integrative Bioscience, National Institutes of Natural Sciences, Higashiyama 5-1, Myodaiji, Okazaki, Aichi 444-8787, Japan

⁴  Center for Biotechnology and Genomic Medicine, Medical College of Georgia, 1120 15th Street, CA4098, Augusta, GA 30912, USA

author email corresponding author email

Molecular Pain 2008, 4:22doi:10.1186/1744-8069-4-22

Published:	5 June 2008

Abstract

Breathing cold air without proper temperature exchange can induce strong respiratory autonomic responses including cough, airway constriction and mucosal secretion, and can exacerbate existing asthma conditions and even directly trigger an asthma attack. Vagal afferent fiber is thought to be involved in the cold-induced respiratory responses through autonomic nerve reflex. However, molecular mechanisms by which vagal afferent fibers are excited by cold remain unknown. Using retrograde labeling, immunostaining, calcium imaging, and electrophysiological recordings, here we show that a subpopulation of airway vagal afferent nerves express TRPM8 receptors and that activation of TRPM8 receptors by cold excites these airway autonomic nerves. Thus activation of TRPM8 receptors may provoke autonomic nerve reflex to increase airway resistance. This putative autonomic response may be associated with cold-induced exacerbation of asthma and other pulmonary disorders, making TRPM8 receptors a possible target for prevention of cold-associated respiratory disorders.