Table 1.
Modulation of gastrointestinal 5-HT in murine motility models
| Model | Effect | Findings (Compared With Control) | |
|---|---|---|---|
| Heredia et al. (51) and Li et al. (75) | TPH1KO mice | Lack EC cell-derived 5-HT (intestinal mucosa) | Elongated colon; poorly disseminated CMMCs that moved in retrograde fashion; lack of response to 5-HT3 antagonist, ondansetron (51); no change in in vivo motility (75) |
| Israelyan et al. (61) | TPH2-R439H mice | Reduced neuronal 5-HT (CNS and ENS) | Slower in vivo motility; slower and less frequent CMMC compared with WT; decreased neuronal number in ENS |
| Li et al. (75) | TPH2KO mice | Lack neuronal 5-HT (CNS and ENS) | Slowed in vivo motility; fewer enteric neurons |
| Margolis et al. (83) | SERT Ala56 mice | Increased 5-HT inactivation → decreased 5-HT availability (CNS and ENS) |
Slower and less frequent CMMCs; fewer enteric neurons |
| Margolis et al. (83) | SERT KO mice | Decreased 5-HT inactivation → increased 5-HT availability (CNS and ENS) |
Faster and more frequent CMMCs compared with WT; increased neurogenesis |
| Margolis et al. (83) | Fluoxetine exposed | Inhibition of SERT; increased 5-HT availability | Slowed in vivo motility; faster and more frequent CMMCs compared with WT; increased enteric neurons |
5-HT, serotonin (5-hydroxytryptamine); CNS, central nervous system; CMMC, colonic migrating motor complexes; EC, endothelial cell; ENS, enteric nervous system; KO, knockout; SERT, serotonin reuptake transporter; TPH, tryptophan hydroxylase; WT, wild type.