Sexual characteristics of high-temperature sterilized male Mozambique tilapia, Oreochromis mossambicus.

INTRODUCTION: In order to clarify the effect of extremely high temperature on gonads of fish, juveniles of the Mozambique tilapia, Oreochromis mossambicus, at three days after hatching (d.a.h.) were reared at a high temperature (37 ± 0.5 °C) for 50 days. The heat-treated fish were then cultivated at a normal water temperature for over six months. RESULTS: The testes of all individuals heat-treated for 50 days were sterile. Histological analysis revealed the complete absence of all stages of spermatogenic germ cells in the testes of the heat-treated males; however, structures within a layer of epithelial cells lining the efferent ducts were observed to actively secrete sperm fluid into the ducts, as in the mature testes of normal males. Clusters of cells immunopositive against P450scc and 3ß-hydroxysteroid dehydrogenase were observed in the sterilized testes. Leydig cells had developed smooth endoplasmic reticulum and several mitochondria with tubular cristae indicating active steroidogenesis. The sterilized males displayed male nuptial coloration, actively dug spawning nests, and mated with normal mature females. However, females mated with these males initially brooded their eggs normally but released them prematurely at 4-5 days. All the released eggs were unfertilized and dead. CONCLUSION: Heat-sterilized male tilapia matures endocrinologically but completely lacks spermatogenic germ cells.

Evidence that IP3 and ryanodine-sensitive intra-cellular Ca2+ stores are not involved in acute hyposmotically-induced prolactin release in Tilapia.

Prolactin (PRL) cells from the euryhaline tilapia, Oreochromis mossambicus, behave like osmoreceptors by responding directly to reductions in medium osmolality with increased secretion of the osmoregulatory hormone PRL. Extracellular Ca(2+) is essential for the transduction of a hyposmotic stimulus into PRL release. In the current study, the presence and possible role of intracellular Ca(2+) stores during hyposmotic stimulation was investigated using pharmacological approaches. Changes in intracellular Ca(2+) concentration were measured with fura-2 in isolated PRL cells. Intracellular Ca(2+) stores were depleted in dispersed PRL cells with thapsigargin (1 microM) or cyclopiazonic acid (CPA, 10 microM). Pre-incubation with thapsigargin prevented the rise in [Ca(2+)](i) induced by lysophosphatidic acid (LPA, 1 microM), an activator of the IP(3) signalling cascade, but did not prevent the hyposmotically-induced rise in [Ca(2+)](i) in medium with normal [Ca(2+)] (2mM). Pre-treatment with CPA produced similar results. Prolactin release from dispersed cells followed a pattern that paralleled observed changes in [Ca(2+)](i). CPA inhibited LPA-induced prolactin release but not hyposmotically-induced release. Xestospongin C (1microM), an inhibitor of IP(3) receptors, had no effect on hyposmotically-induced PRL release. Pre-exposure to caffeine (10mM) or ryanodine (1microM) did not prevent a hyposmotically-induced rise in [Ca(2+)](i). Taken together these results indicate the presence of IP(3) and ryanodine-sensitive Ca(2+) stores in tilapia PRL cells. However, the rapid rise in intracellular [Ca(2+)] needed for acute PRL release in response to hyposmotic medium can occur independently of these intracellular Ca(2+) stores.