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Howard Hughes Medical Institute, Departments of Cell Biology and Medicine, Division of Gastroenterology, Duke University Medical Center, Durham, North Carolina 27710
The mechanisms by which dopamine (DA)
influences gastrointestinal (GI) tract motility are incompletely
understood and complicated by tissue- and species-specific differences
in dopaminergic function. To improve the understanding of DA action on
GI motility, we used an organ tissue bath system to characterize motor
function of distal colonic smooth muscle segments from wild-type and DA
transporter knockout (DAT 
/) mice. In wild-type mice, combined
blockade of D1 and D2 receptors resulted in
significant increases in tone (62 ± 9%), amplitude of spontaneous
phasic contractions (167 ± 24%), and electric field stimulation
(EFS)-induced (40 ± 8%) contractions, suggesting that endogenous
DA is inhibitory to mouse distal colonic motility. The amplitudes of
spontaneous phasic and EFS-induced contractions were lower in DAT /
mice relative to wild-type mice. These differences were eliminated by
combined D1 and D2 receptor blockade,
indicating that the inhibitory effects of DA on distal colonic motility
are potentiated in DAT / mice. Motility index was decreased but
spontaneous phasic contraction frequency was enhanced in DAT / mice
relative to wild-type mice. The fact that spontaneous phasic and
EFS-induced contractile activity were altered by the lack of the DA
transporter suggests an important role for endogenous DA in modulating
motility of mouse distal colon.
transgenic mice; motility index; dopamine receptor antagonists; electric field stimulation; peripheral hyperdopaminergia
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