Ecdysis of the Trophotaenial Placenta in Neonates of Viviparous Goodeid Fishes

ULUKOY, Gulsen; WOURMS, John P*; Mugla Univ., Turkey; Clemson Univ., SC USA: Ecdysis of the Trophotaenial Placenta in Neonates of Viviparous Goodeid Fishes

Trophotaeniae, external extensions of the hindgut are the chief site of maternal nutrient uptake in embryos of viviparous goodeid fishes. At birth, neonates leave the isosmotic maternal environment for a hyposmotic one. Transport functions of trophotaeniae, formerly beneficial, now are an osmotic liability. Trophotaeniae are ecdysed, detaching at the terminal end of the gut. Studies of the term embryos of Ameca splendens, excised from females and incubated at different osmotic and ionic conditions reveal that hyposmotic shock triggers ecdysis. Embryos in isosmotic saline retain functional trophotaeniae for over 14 days. In hyposmotic saline, trophotaenial circulation ceases almost immediately and ecdysis occurs in a few hours, There is no evidence of a discrete apoptotic zone of autotomy. The incidence of apoptosis is low and not localized. We postulate that osmotic shock and circulatory arrest triggers cellular necrosis which produces a systematic weakening of tissue structure. Mechanical breakage occurs at the junction between embryo and trophotaeniae where the force generated by the swimming neonate is resisted by the drag created by the massive (135 mm2) surface area of the trophotaeniae that act as a “sea anchor.” After ecdysis, terminal gut and adjacent epidermal tissues undergo reorganization and an ectoderm-lined proctodaeum replaces the endoderm-lined vent. There is a distinct line of demarcation between hindgut cells with apical microvilli and proctodaeal cells with apical microplicae. (Supported by NSF) wjohn@clemson.edu

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