Regulation of longitudinal esophageal motility in the house musk shrew (Suncus murinus)

- This study was to clarify components that regulate esophageal motility in the suncus.
- Vagal accetylcholine induced longitudinal contraction in the suncus esophagus.
- Non-cholinergic transmitters evoked longitudinal contraction in the suncus esophagus.
- Non-cholinergic transmitters were released from mast cells.
- Longitudinal contraction might contribute to esophageal shortening during emesis.

Suncus murinus (house musk shrew; suncus) is a species of insectivore that has an ability to vomit. Although longitudinal movement of the esophagus would be related to the emetic response, regulatory mechanisms for the suncus esophageal motility are unclear. Therefore, the aim of the present study was to clarify components that regulate esophageal motility in the suncus. An isolated segment of the suncus esophagus was placed in an organ bath, and longitudinal mechanical responses were recorded using a force transducer. Electrical stimulation of the vagus trunk evoked a biphasic contractile response. The first phase of the contractile response was blocked by α-bungarotoxin, a blocker of nicotinic acetylcholine receptors on striated muscle cells, whereas the second one was blocked by atropine, a blocker of muscarinic acetylcholine receptors on smooth muscle cells. Next, we investigated whether mast cells are involved in motor functions of the suncus esophagus. Application of a mast cell stimulator, compound 48/80, elicited contractile responses, which was resistant to tetrodotoxin. Exogenous application of serotonin and histamine induced contractile responses. The mast cell activation-mediated contraction was abolished by double desensitization by serotonin and histamine and pre-treatment with indomethacin, a cyclooxygenase inhibitor. The findings show that cholinergic and non-cholinergic transmitters induce longitudinal contraction in the suncus esophagus, which might contribute to esophageal shortening during emesis. Cholinergic transmitters are derived from vagal efferents, and non-cholinergic transmitters, which are thought to be serotonin, histamine and prostaglandins, are released from mast cells.