Pulmonary expression of mechanogated K2P channels with special reference to the neuroepithelial body micro‐environment

Abstract

The two‐pore‐domain K+ (K2P) channels TREK and TRAAK are gated by mechanical stimuli. Recently, we suggested the potential involvement of neuroepithelial bodies (NEBs) in mechanotransduction from the airways. NEBs are structurally well‐defined airway receptors composed of groups of neuroendocrine airway epithelial cells that receive at least two different populations of myelinated vagal afferent nerve terminals. Physiological evidence, but lack of neurochemical characterization of several classes of vagal mechanosensitive airway receptors, prompted us to focus on the expression of mechanogated K2P ion channels in mouse airways and more in particular in the NEB micro‐environment. TREK‐1 immunoreactivity was found in the lungs but seemed to be restricted to airway smooth muscle cells. TRAAK on the other hand appeared to be mainly expressed in the terminals of vagal myelinated nerves, both intraepithelially in NEBs and in so‐called smooth muscle associated airway receptors (SMARs). The observation that the extensive terminals of vagal myelinated afferents in NEBs reveal intrinsic mechanosensitive properties strengthens our hypothesis that, in addition to SMARs, the NEB micro‐environment likely accounts for subpopulations of the electrophysiologically characterized vagal airway mechanosensors.Support: FWO grants G.0085.04 and G.0081.08 (DA); UA grants GOA BOF 2007 (DA) and KP BOF 2006 (IB)