Short-Term Steroid Treatment on Plasma LH and FSH in Castrated Rats from Birth to Puberty

Ojeda, Sergio R.; Ramírez, Victor D.

doi:10.1159/000122201

Cited by 38 publications

(12 citation statements)

References 6 publications

(8 reference statements)

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“…A nearly physiological dose of Eb injected for 4 days in short-term ovariectomized infantile rats failed to decrease plasma FSH titers [Ojeda and R amirez, 1973] although FSH did increase after ovariectomy [Ramirez, 1972a], This finding was interpreted as indicating a relative insensitivity of the estrogen negative feedback at that age. Such a feedback can indeed be demonstrated in the infantile rat [MEUS-RoELOFse/a/., 1973;CALiGARise/a/., 1972], as revealed by the increased gonadotropin levels that followed ovari ectomy.…”

Section: Discussionmentioning

confidence: 99%

Further Studies on the Maturation of the Estrogen Negative Feedback on Gonadotropin Release in the Female Rat

Ojeda¹,

Kalra

McCann

1975

Neuroendocrinology

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To evaluate estrogen negative feedback in infantile female rats, 9-day-old rats were ovariectomized (OVX) and treated with different doses of estradiol benzoate (Eb, s.c. once daily for 2 days); plasma LH, FSH and estradiol (E₂) levels were then determined by RIA. The responses of these rats were compared with those of 25-day-old rats subjected to the same experimental procedures. In intact sham-operated controls, plasma FSH was elevated on days 9–13 and low on days 25–29, whereas LH did not change significantly throughout the period studied. OVX at day 9 or 25 increased the levels of both hormones, with the response faster and larger in the older rats. Treatment with Eb was more effective in suppressing the post-castration rise in gonadotropin levels in 27-day-old than in 11-day-old rats. At day 27 plasma E₂ was elevated to pre-castration values by as little as 10 ng of Eb, whereas at day 11 this dose produced plasma E₂ titers even higher than pre-castration values. Plasma E₂ titers were high at 9–13 days of age and low at days 25–29. OVX on day 9 decreased E₂ 2–4 days later to about ½ the initial concentration, whereas adrenalectomy (ADRX) or ADRX-OVX was followed by an almost complete disappearance of the steroid. When E₂ was injected at day 10 in intact rats to elevate plasma E₂, E₂ remained elevated when measured 3 to 120 min after its injection, but on day 25, 50% of the injected E₂ had disappeared from plasma in 90 min. These results provide additional support for the view that estrogen negative feedback, even though present in infantile rats, is less effective than later in life and hence indicate that high gonadotropin titers observed at days 9–13 in the presence of high E₂ may be caused by the relative ineffectiveness of the feedback at these early ages. The high E₂ titers appear to be caused by an enhanced rate of production of E₂ by the adrenals and ovaries and by a reduced metabolic clearance of the steroid.

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Section: Discussionmentioning

confidence: 99%

Further Studies on the Maturation of the Estrogen Negative Feedback on Gonadotropin Release in the Female Rat

Ojeda¹,

Kalra

McCann

1975

Neuroendocrinology

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“…During neonatal and infantile days the negative feed back effects of E2 are hampered [9, 51,59] by the presence of elevated levels of alpha-fetoprotein which binds estrogens tightly [69]. At this time the predominant negative feedback signal is provided by androgens [14].…”

Section: Steroid Negative Feedbackmentioning

confidence: 99%

“…At this time the predominant negative feedback signal is provided by androgens [14]. As levels of alpha-feto protein decline, the effectiveness of E2 increases [9, 51,59], becoming maximal during juvenile days [9,14]. The capaci ty of E2 to keep gonadotropin secretion in check remains fully operative unitl the very day of first proestrus [9].…”

Section: Steroid Negative Feedbackmentioning

confidence: 99%

Neuroendocrine Mechanisms Controlling the Onset of Female Puberty:The Rat as a Model

1983

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The advent of female puberty represents the culmination of a diversity of developmental processes which affect all components of the reproductive axis. Development of neuroendocrine reproductive functions proceeds in a harmonious and interrelated manner. No unique ‘trigger’ of puberty can be discerned, but rather puberty represents the climax of a cascade of events, finely interconnected throughout the continuum of sexual maturation. A resetting of the hypothalamic ‘gonadostat’ to steroid negative feedbak appears to be a phenomenon associated with puberty, but not its cause. Although the central nervous system plays a pivotal role in the development of the ovary, it is the acquisition of ovarian ovulatory capacity which finally determines the timing of the first preovulatory surge of gonadotropins. In contrast to primates, development of the central component of estradiol positive feedback is an early event in the female rat. However, in most species – including the rat – amplification (or initiation) of a particular, synchronous pattern of LHRH release appears essential for the initiation of puberty. The mechanisms underlying this functional change of the LHRH secreting system are not clearly understood. In the rat, ovarian development proceeds under the influence of gonadotropins, and the somatomammotropins PRL and GH. More intriguingly, evidence is now emerging that the central nervous system may convey direct information to the ovary via the ovarian nerves, thus providing a hormone-independent fine tuning for its control. Upon reaching adequate development, the ovary through its secretory products, acts on an already competent hypothalamic-pituitary axis to activate the central component of estradiol positive feedback. This phenomenon, visualized as accelerated function of a mature neurotransmitter-LHRH circuitry brings about the first preovulatory LHRH surge. Serum LH and FSH levels increase abruptly and the first ovulation then ensues.

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“…On the basis of early findings (Donovan & van der Werff ten Bosch, 1959) and those obtained from steroid replacement studies after gonadectomy (Ojeda & Ramirez, 1973 ;Steele & Weisz, 1974), the concept grew that as maturity progressed there was a decrease in sensitivity of brain-pituitary mech¬ anisms to negative feedback, and that this might in some way account for the onset of puberty. However, Odell & Swerdloff (1976) have found that testosterone treatment, initiated on the day of castration, lowers serum LH concentrations equally well in 10-and 21 -day-old as in 73-day-old males ; the dose of testosterone required to lower post-castration FSH values was smaller in the youngest animals, although similar doses were required for 21-and 75-day-old animals.…”

Section: Negative Feedbackmentioning

confidence: 99%

Reflections on the attainment of puberty in the rat: have circadian signals a role to play in its onset?

Mackinnon¹,

Puig-Duran²,

Laynes³

1978

Reproduction

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Short-Term Steroid Treatment on Plasma LH and FSH in Castrated Rats from Birth to Puberty

Cited by 38 publications

References 6 publications

Further Studies on the Maturation of the Estrogen Negative Feedback on Gonadotropin Release in the Female Rat

Further Studies on the Maturation of the Estrogen Negative Feedback on Gonadotropin Release in the Female Rat

Neuroendocrine Mechanisms Controlling the Onset of Female Puberty:The Rat as a Model

Reflections on the attainment of puberty in the rat: have circadian signals a role to play in its onset?

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