Evidence that signal transduction for osmoreception is mediated by stretch-activated ion channels in tilapia.

Prolactin (PRL) plays a central role in the freshwater osmoregulation of teleost fish, including the tilapia (Oreochromis mossambicus). Consistent with this action, PRL release from the tilapia pituitary increases as extracellular osmolality is reduced both in vitro and in vivo. Dispersed tilapia PRL cells were incubated in a perfusion chamber that allowed simultaneous measurements of cell volume and PRL release. Intracellular Ca(2+) concentrations were measured from fura 2-loaded PRL cells treated in a similar way. Gadolinium (Gd(3+)), known to block stretch-activated cation channels, inhibited hyposmotically induced PRL release in a dose-related manner without preventing cell swelling. Nifedipine, an L-type Ca(2+) channel blocker, did not prevent the increase in PRL release during hyposmotic stimulation. A high, depolarizing concentration of KCl induced a transient and marked increase of intracellular Ca(2+) and release of PRL but did not prevent the rise in intracellular Ca(2+) and PRL release evoked by exposure to hyposmotic medium. These findings suggest that a decrease in extracellular osmolality stimulates PRL release through the opening of stretch-activated ion channels, which allow extracellular Ca(2+) to enter the cell when it swells.