Induction of trypsinogen secretion in herring larvae (Clupea harengus)

Mechanisms initiating trypsinogen secretion were studied in laboratory reared herring larvae (Clupea harengus L.) exposed to physical and chemical stimuli. Pancreatic secretion of trypsinogen was quantified for each stimulus type as the increase above pre-stimulus level of intestinal trypsin content. Larval prey types were: nauplii, copepodites or adult Acartia tonsa, small polystyrene spheres (diameter 94 μm), small (diameter 79 μm) or large (diameter 170 μm) polystyrene-latex spheres. Intestinal trypsin content can be expressed as a function of two variables: meal size and content of pancreatic trypsinogen. Trypsinogen secretion increases with different prey items in the order: small spheres, nauplii and copepodites. Larvae which eat large spheres secrete more enzyme than if fed small spheres but trypsinogen secretion is similar in fish larvae fed copepodites and large spheres. The fact that the size of non-biodegradable particles exerts a major control over trypsinogen secretion suggests neural — as opposed to chemically mediated — initiation of secretion. A cephalic phase of secretory stimulation could not be demonstrated during swallowing of copepods or exposure for 2 to 3 h to compounds which leak from live copepodites. As cephalic and gastric phases of secretory stimulation are absent, initiation of trypsinogen secretion must take place in the intestine. Larval herring retain trypsin in the intestine. Ca. 4.5 h after a meal, 3/4 of the enzyme is located in the intestinal fluid, presumably available for hydrolysis of subsequent meals, and the high proportion (ca. 25%) of the pancreatic trypsinogen content which is secreted for copepodite prey may thus not be energetically wasteful for the larvae.