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Chapter

OVIPOSITION OVULATION

Chapter

OVIPOSITION OVULATION

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OVIPOSITION OVULATION book

OVIPOSITION OVULATION

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OVIPOSITION OVULATION book

BookReproductive Biology and Phylogeny of Chondrichthyes

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Edition 1st Edition
First Published 2005
Imprint CRC Press
Pages 16
eBook ISBN 9780429062902

ABSTRACT

The subject of hormone action on the reproductive tract is considered in Chapter 9 of this volume. The following general comments serve only to

268 Reproductive Biology and Phylogeny of Chondrichthyes

provide a link between the two related subjects. The functions of estradiol (E2), progesterone (P4), and testosterone (T) during gestation and ovarian recrudescence are not fully understood, but enough information is available to indicate that the ovarian hormones regulate reproductive tract function. Relaxin, which has been characterized in elasmobranchs (Bullesbach ef a/. 1987), appears to play a role in connective tissue compliance and is involved in regulating passage of eggs and young from the oviduct, a function that appears to be coordinated by E2, as in mammals. E2 may also be involved in regulating morphological properties of specialized regions of the reproductive tract, such as the "closing device" at the anterior end of the uterus (Koob e/ a/. 1983). Pretreatment with E2 has been shown to potentiate the effect of relaxin and insulin on the size of the cervix and on fetal retention in Squa!us acanlhias (Koob eta/. 1984), probably through a regulatory effect on oviductal relaxin receptors. It is also likely that E2 plays a part in the synthesis of egg capsule precursors (Koob and Callard 1982). Manire et a/. (1995) suggest that elevations of T and related androgens, such as dihydrotestosterone (DHT), may play a part in direct regulation of quiescence of Lhe myometrium and activation of sperm stored in the oviducal gland during the follicular phase. P4 is also thought to play a role in ovulation, encapsulation, and oviposition due to timing of heightened titers, and it may also play a role in egg retention (Koob et a!. 1986). It seems clear that decreasing P4 titres in the second half of pregnancy allows increasing E2 levels to upregulate vitellogenin production in the liver.

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