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. 2018 Oct 1;24(4):643–655. doi: 10.5056/jnm18040

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© 2018 The Korean Society of Neurogastroenterology and Motility

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Influence of MKC-231, a choline uptake enhancer, on high-affinity choline transporter 1 (CHT1) expression and intestinal motility in vivo. (A) Immunoblots (left) and histogram (right) for CHT1 in the colon from control and MKC-231-treated rats showing that the ratios of CHT1 to β-actin expression in control rats are significantly increased after 10 consecutive days of MKC-231 treatment. (B) Merged pictures of immunostaining for CHT1, transmembrane member 16A (TMEM16A), and DAPI (4′,6-diamidino-2-phenylindole) in longitudinal colonic sections from control (left) and MKC-231 rats (right) (×400) revealing that the density of CHT1 labelling in the colonic muscular layer is considerably elevated after treatment with MKC-231. White arrows indicate CHT1-positive intramuscular interstitial cells of Cajal. White arrowheads indicate CHT1-immunoreactive (IR) neurons in the myenteric plexus. (C) The intestinal transit time of MKC-231-rats is reduced compared to that of control rats. (D) The fecal water content of the MKC-231 group is considerably increased compared with that of the control group. *P < 0.05 compared to controls.