Mice lacking the dopamine transporter display altered regulation of distal colonic motility.
Am J Physiol Gastrointest Liver Physiol
; 279(2): G311-8, 2000 Aug.
Article
em En
| MEDLINE
| ID: mdl-10915639
ABSTRACT
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 D(1) and D(2) 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 D(1) and D(2) 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.
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Base de dados:
MEDLINE
Assunto principal:
Proteínas de Membrana Transportadoras
/
Glicoproteínas de Membrana
/
Proteínas de Transporte
/
Colo
/
Motilidade Gastrointestinal
/
Proteínas do Tecido Nervoso
Limite:
Animals
Idioma:
En
Ano de publicação:
2000
Tipo de documento:
Article