Vitellogenesis level and induction of maturation in the ovary of the Blue GouramiTrichogaster trichopterus (Anabantidae, Pallas, 1770)

✍ Scribed by Degani, Gad ;Boker, Rachel

• Publisher: John Wiley and Sons
• Year: 1992
• Tongue: English
• Weight: 963 KB
• Volume: 263
• Category: Article
• ISSN: 0022-104X
• DOI: 10.1002/jez.1402630313

✦ Synopsis

Abstract

The effectiveness of 17α‐hydroxyprogesterone (17‐P), 17α,20β‐dihydroxy‐4‐pregnen‐3‐one (17,20‐P), and carp gonadotropin (cGtH) in inducing germinal vesicle breakdown (GVBD) was examined in vitro in female blue gourami Trichogaster trichopterus (Pallas, 1770) as a model of multispawning, asynchronic fish. Induced GVBD was measured at three stages of ovary development: low (<25%), intermediate (≈30%), and high vitellogenesis (>45%).

The size of oocytes increased rapidly from the chromatin nucleolar stage to the stage of vitellogenesis, but little more thereafter. The effect of the hormones was to pass the oocytes from stage to stage, with very little effect on the size during maturation.

Only slight influence was detected on ovaries with a low percentage of vitellogenesis by treatment with 17‐P, 17,20‐P, cGtH, or any combination of these hormones.

In the intermediate percentage range, cGtH effected an increase in vitellogenesis, while cGtH in combination with 17‐P or 17,20‐P induced a low percentage of GVBD.

In ovaries with a high percentage of vitellogenesis (>45%), in vitro treatment with 100 ng/ml cGtH had little effect, 300 ng/ml cGtH significantly increased vitellogenesis, and 600 ng/ml induced a low level of GVBD. In vitro treatment with 300 ng/ml cGtH and various concentrations of 17‐P caused a significant increase in the percentage of oocytes in GVBD, and even induced ovulation. Various combinations of cGtH, 17‐P, and 17,20‐P significantly increased the percentage of oocytes in maturation, and also caused ovulation.

A model of the relationship between sexual behavior, ovary development, and control by MIS and GtH in this type of fish is discussed. © 1992 Wiley‐Liss, Inc.