A novel postsynaptic signal pathway of sympathetic neural regulation of murine colonic motility

Transcriptome data revealed alpha1 adrenoceptors (ARs) expression in platelet-derived growth factor receptor alpha(+) cells (PDGFRalpha(+) cells) in murine colonic musculature. The role of PDGFRalpha(+) cells in sympathetic neural regulation of murine colonic motility was investigated. Norepinephrine (NE), via alpha1A ARs, activated a small conductance Ca(2+) -activated K(+) (SK) conductance, evoked outward currents and hyperpolarized PDGFRalpha(+) cells (the alpha1A AR-SK channel signal pathway). alpha1 AR agonists increased intracellular Ca(2+) transients in PDGFRalpha(+) 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 alpha1A AR-SK channel signal pathway. Postsynaptic signaling through alpha1A ARs in PDGFRalpha(+) cells is a novel mechanism that conveys part of stress responses in the colon. PDGFRalpha(+) cells appear to be a primary effector of sympathetic neural regulation of murine colonic motility.