E-Book, Englisch, 308 Seiten
Martini / James Current Topics in Experimental Endocrinology
1. Auflage 2013
ISBN: 978-1-4832-1733-8
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)
Volume 1
E-Book, Englisch, 308 Seiten
ISBN: 978-1-4832-1733-8
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)
Current Topics in Experimental Endocrinology, Volume 1 provides a review on experimental endocrinology. The book discusses the basic concepts of saturation analysis techniques; the concept of how steroid hormones might influence the differentiation of certain brain structures instrumental in the control of gonadotropin secretion; and trends in the physiology of the posterior pituitary. The text also describes role of thymosin and other thymic factors in the development, maturation, and functions of lymphoid tissue; the chemistry and comparative chemistry of calcitonin, factors affecting its secretion and metabolic degradation, and the results of its preliminary therapeutic application in the complex situation of disordered bone metabolism found in Paget's disease. The chemical nature and the importance of the long-acting thyroid stimulator; the endocrinological implications of prostaglandins; and effects of ovarian hormones at the subcellular level are also encompassed. Endocrinologists and students taking related courses will find the book invaluable.
Autoren/Hrsg.
Weitere Infos & Material
Steroid Hormones and the Differentiation of the Central Nervous System
Béla Flerkó, Department of Anatomy, University Medical School, Pécs, Hungary
Publisher Summary
This chapter discusses the concept of the way steroid hormones might influence the differentiation of certain brain structures instrumental in the control of gonadotropin secretion. The concept invokes dual mechanism for the neural control of the secretion of gonadotropic hormones (GTH). The first, termed as the tonic mechanism, stimulates a tonic, basal discharge of follicle-stimulating (FSH) and luteinizing hormone (LH). Tuberoinfundibular neurons in the hypophysiotropic area (HTA) of the hypothalamus, which produce FSH- and LH-releasing factors (FRF and LRF), are responsible for this mechanism. The second mechanism modulates the activity of the FRF- and LRF-producing neurons. This involves brain structures outside the HTA, and may be termed a cyclic mechanism, being indispensable for the maintenance of the cyclic release of FRF–FSH and LRF–LH, respectively. Hypothalamic parts of the cyclic mechanism are the preoptic LH trigger and the anterior hypothalamic FSH control mechanism. A number of experimental data indicate that the neurons contributing to the hypothalamic FSH and LH control mechanisms are instrumental in the neurohormonal steroid feedback controlling cyclic gonadotropin release.
II The Androgen-Sterilized Rat
III The Possible Site of Action of Androgen
A A Dual Hypothalamic Mechanism Controlling Gonadotropin Secretion
C Data Suggesting That Hypothalamic LH and FSH Mechanisms Are Deranged in the Androgen-Sterilized Rat
IV The Possible Mechanism of Action of Androgen
A Characteristic Pattern of Uptake and Retention of Tritiated Estradiol by Certain Hypothalamic Areas
V Effects of Neonatal Treatment with Steroid Hormones Other Than Androgen on Subsequent Fertility
A The POS Induced by Neonatal Estrogen Administration
B Anestrous State Induced by Neonatal Estrogen Treatment
C Other Steroid Hormones Inducing Sterility in the Rat When Administered Neonatally
I General Introduction
It is not the purpose of this review to cover the whole field indicated by the title. Rather, this contribution will summarize what the author considers to be pertinent studies that have led him to a concept of how steroid hormones might influence the differentiation of certain brain structures instrumental in the control of gonadotropin secretion. These studies were carried out mainly on androgen-sterilized rats. Modifications in reproductive function after exposure to steroid hormones during the neonatal period were recently summarized by Barraclough (1967), and this excellent review is particularly helpful in that pertinent studies carried out before 1967 can be treated very briefly in this chapter.
II The Androgen-Sterilized Rat
A The Polyfollicular Ovary Syndrome (POS) Induced by Perinatal Administration of Androgen
It has long been known that the ovary transplanted to any region of the male rat, except the spleen, does not develop a corpus luteum. Pfeiffer (1936) was the first to observe that ovaries grafted to adult intact female rats or to adult male rats which had been castrated at birth showed normal follicular development and formation of corpora lutea. However, when testes were implanted into newborn females, the ovaries of these animals, when they became adults, contained only growing follicles and interstitial tissue without a corpus luteum (the so-called polyfollicular ovary), and persistent vaginal cornification ensued after puberty.
It turned out later on that the condition of polyfollicular ovary associated with persistent vaginal cornification and permanent sterility, termed the polyfollicular ovary syndrome, could be induced by administration of testosterone given repeatedly from birth or 6 days of age to either 5–6 or 25 weeks of age (Shay ., 1939; Bradbury, 1941).
To evaluate more carefully the effect and duration of effect of a hormone administered at a given time in development, Barraclough and Leathern (1954) and Barraclough (1955) using the mouse, and Barraclough (1961) using the rat, studied the effect of a single injection of testosterone given in the first 20 days of life. As a consequence of these studies, Barraclough (1961) assumed that there is a “critical period” in the development of the female mouse and rat during the first 10 days of life when injection of a single 1.25-mg dose of testosterone will induce subsequent anovulatory sterility associated with the POS.
B Effect of Age and Dosage
Androgen treatment at 10 days of age had a less drastic effect, as the ovaries of only 4 of 10 rats lacked corpora lutea at 100 days of age. In mice treated at 10 days of age, ovulation was delayed approximately 10 days, but at 60 days of age 85% of the ovaries contained corpora lutea as compared with 90% of the littermate controls. All ovaries of rats or mice treated with androgen at 20 days of age were normal at autopsy (Barraclough, 1967).
While 99.8% of the rats treated with a single injection of 1.25 mg of testosterone propionate (TP) at 5 days of age, were sterile, as little as 10, 5, or 1 µg, administered on day 5, produced sterility in 70.6, 44.0, and 30.0%, respectively, of the treated rats (Barraclough, 1961; Gorski and Barraclough, 1963).
Later, it became clear that a delineation of the “critical period” is complicated by several variables as Swanson and van der Werff ten Bosch (1964b) pointed out. They showed that the full “early androgen” syndrome may not exist at the time of puberty but may develop after an initial period of normal female ovarian activity (Swanson and van der Werff ten Bosch, 1964a,b). Second, the relation between the time of androgen administration and the effect on reproductive function is greatly influenced by variations in the dose of androgen administered. In other words, as maturation of the brain–pituitary–gonadal axis proceeds with age (from 1 to 10 days of age), “masculinization” may still be produced, provided that the dosage of administered androgen is increased. Similar observations were reported also by Gorski (1968) and Kurcz (1969; Kurcz and Gerhardt, 1968).
The effects of androgen administered prior to birth on subsequent fertility have also been studied. After a single dose of 2.5 mg of TP into pregnant rats, Swanson and van der Werff ten Bosch (1964b) did not observe any alteration in the cyclic pattern of gonadotropin secretion of the female offspring. They interpreted their finding to mean that androgen given to the mother animal did not pass, presumably, the placental barrier in such a measure that it could get into the fetuses in an effective amount. Obviously, the amount of androgen injected into pregnant rats was insufficient, since Swanson and van der Werff ten Bosch (1965) gave an account of successful treatment in their next paper. A single dose of 10–25 mg of TP given to pregnant rats, or injection of 20–100 µ TP into the fetuses, did convert the female (cyclic) hormonal pattern into a male (acyclic) pattern. Flerkó . (1967) also observed the masculinizing effect of TP injected either directly into fetuses or into pregnant rats.
1 TP Injection into Fetuses
Nineteen females were anesthetized on day 19 of pregnancy, and the uterus was exposed. All fetuses were injected with 0.5 mg of TP. Thirteen out of the 19 aborted shortly after operation. The remaining 6 pregnant...
