Proceedings for Annual Meeting of The Japanese Pharmacological Society
Online ISSN : 2435-4953
The 95th Annual Meeting of the Japanese Pharmacological Society
Session ID : 95_2-O-093
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Oral Sessions
Sympathetic neuronal mechanisms in the regulation of mouse colonic motility.
*Yoshihiko KitoMasaaki Kurahashi
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Abstract

Morphological study revealed that sympathetic neurons are closely associated with PDGFRα + cells in mouse colonic musculature. In addition, gene expression study showed that α1A adrenoceptors (α1A ARs) are expressed exclusively in PDGFRα + cells of mouse colon. Therefore, we investigated how sympathetic neurons regulate mouse colonic motility via α1A ARs in PDGFRα + cells. Noradrenaline (NAd), via α1A ARs, activated a small conductance Ca2+-activated K+ (SK) channels and hyperpolarized a single PDGFRα + cell (the α1A AR – SK channel signal pathway), resulting in hyperpolarization of neighboring smooth muscle cells (SMCs) connected by gap junctions, leading to inhibition of spontaneous contractions of colonic muscle. Sympathetic nerve stimulation (SNS) inhibited propulsive contractions represented by the colonic migrating motor complexes (CMMCs) via the α1A AR – SK channel signal pathway in wild type mouse, however CMMCs were not affected by SNS in the colon of Adra1a−/− mouse. These results suggest that NAd released from sympathetic neurons inhibited mouse colonic motility via the α1A AR – SK channel signal pathway in PDGFRα + cells.

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