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

Transcriptome data revealed alpha 1 adrenoceptors (ARs) expression in platelet-derived growth factor receptor alpha(+) cells (PDGFR alpha(+) cells) in murine colonic musculature. The role of PDGFR alpha(+) cells in sympathetic neural regulation of murine colonic motility was investigated. Norepinephrine (NE), via alpha 1A ARs, activated a small conductance Ca2+-activated K+ (SK) conductance, evoked outward currents and hyperpolarized PDGFR alpha(+) cells (the alpha 1A AR-SK channel signal pathway). alpha 1 AR agonists increased intracellular Ca2+ transients in PDGFR alpha(+) 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 alpha 1A AR-SK channel signal pathway. Postsynaptic signaling through alpha 1A ARs in PDGFR alpha(+) cells is a novel mechanism that conveys part of stress responses in the colon. PDGFR alpha(+) cells appear to be a primary effector of sympathetic neural regulation of murine colonic motility.