A novel postsynaptic signal pathway of sympathetic neural regulation of murine colonic motility
Masaaki Kurahashi, Yoshihiko Kito, Salah A. Baker, Libby K. Jennings, James G. R. Dowers, Sang Don Koh, Kenton M. Sanders
Abstract
Abstract Transcriptome data revealed α1 adrenoceptors (ARs) expression in platelet‐derived growth factor receptor α + cells (PDGFRα + cells) in murine colonic musculature. The role of PDGFRα + cells in sympathetic neural regulation of murine colonic motility was investigated. Norepinephrine (NE), via α1A ARs, activated a small conductance Ca 2+ ‐activated K + (SK) conductance, evoked outward currents and hyperpolarized PDGFRα + cells (the α1A AR‐SK channel signal pathway). α1 AR agonists increased intracellular Ca 2+ transients in PDGFRα + cells and inhibited spontaneous phasic contractions (SPCs) of colonic muscle through activation of a SK conductance. Sympathetic nerve stimulation inhibited both contractions of distal colon and propulsive contractions represented by the colonic migrating motor complexes (CMMCs) via the α1A AR‐SK channel signal pathway. Postsynaptic signaling through α1A ARs in PDGFRα + cells is a novel mechanism that conveys part of stress responses in the colon. PDGFRα + cells appear to be a primary effector of sympathetic neural regulation of murine colonic motility.