Gastrointestinal (GI) Motility is Unaltered by Feeding in Zebrafish

Abstract

Gastrointestinal motility patterns in humans are not constant and respond to the luminal contents and nutrient status (Degen and Phillips, 1996). The zebrafish is a new model system for human GI motility and regulation of motility patterns appears to be controlled by enteric neurons and interstitial cells of Cajal (Huizinga et al., 1995, Farrugia et. al., 2003, Sanders et.al., 2006, Rich et. al., 2007). Although several research laboratories investigate GI motility in zebrafish larvae, no standard protocol for feeding exists and experiments may be performed on fasted or fed larvae. The goal of this study was to examine the effects of feeding on GI motility when ICC and enteric neurons are developed and regulate GI motor patterns in larvae, at 7 days post fertilization ( dpt) (Rich et. al., 2007). Larvae were fasted or fed once daily beginning at 5 dpf. At 7 dpf larvae were fed dry food labeled with FITC-dextran and GI motility was measured using time-lapse imaging and image analysis techniques. Motility was examined in the anterior and the posterior regions of the GI tract. No differences were observed in fish standard length, a developmental marker. The total number and distance of contractions increased in the anterior intestine after feeding. These data suggest that feeding has little influence on GI motility patterns in the posterior intestine. The effects of Cisapride, a prokinetic in humans, was examined and found to increase the contraction number, velocity, and interval. The effects of Niflumic Acid and DIDS were also examined, because anoctamin 1 (ANOl), a chloride-selective channel, has recently been identified as a potential regulator for ICC pacemaker function. Both drugs dramatically reduced the total number of contractions as well as the GI motility index indicating a reduction in coordinated motility patterns. Cisapride, Niflumic Acid, and DIDS have similar effects on GI motility in mice and in the zebrafish, suggesting that similar molecular mechanisms regulate GI motility in zebrafish and mice. The findings contribute to the validation of the zebrafish model system for human GI motility function.