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ABSTRACT
Administration of pregnant mare serum gonadotrophin (PMSG) to peripubertal rats, aged 27 days, induces ovulation provided the animals weigh more than 60 g at the time of the injection. In an attempt to determine whether the apparent immaturity of the ovaries in smaller rats is associated with an inability of the pituitary gland to secrete LH, the biological and immunological properties of LH in peripubertal PMSG-treated rats were examined. A single injection of PMSG caused a marked hypersecretion of LH in rats aged 27 days. The LH in the plasma of rats weighing more than 60 g was active in both the radioimmunoassay and the cytochemical bioassay but that in smaller rats was active only in the former. Plasma from both groups of rats stimulated the release of testosterone from dispersed Leydig cells.
Luteinizing hormone-releasing hormone stimulated the secretion, in vitro, of immunoreactive, cytochemically active LH by pituitary tissue from rats weighing over 60 g. The LH released in vitro from tissue from the smaller animals, like that in their plasma, was active in the radioimmunoassay but not in the cytochemical system. The results suggest that an abrupt change in the nature of LH occurs at puberty and that ovulatory cycles commence only when the pituitary gland secretes the adult form of LH with a full spectrum of biological activity.
J. Endocr. (1985) 104, 173–177
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ABSTRACT
This review emphasizes the heterogeneous structure of the gonadotrophin hormones and the influence of different oligosaccharide structures on the bioactivity of these hormones. A summary has been made of the changes in biopotency of the gonadotrophins throughout the life-cycle of the human and in different endocrine states in the rat.
In general it appears that the charge of the gonadotrophin conferred by the acid radicals attached to the terminal groups on the oligosaccharide structures strongly influences biopotency. Basic structures have a greater potency in in-vitro assays, but a short half-life in the circulation, while acidic isoforms are less potent, but have a longer circulatory time and are thus more active in in-vivo estimations. More basic forms are secreted over the adult reproductive years compared with the prepubertal period and old age. The glycosyl structure of the carbohydrate groups also alters in different endocrine states and is probably also important for the bioactivity and potency of the hormone.
Gonadotrophin-releasing hormone (GnRH) and gonadal steroids can influence the type of isoform synthesized and released, and therefore affect the function of gonadotrophins. GnRH enhances glycosylation, sulphation and biopotency. Oestradiol potentiates the glycosylation induced by GnRH and reduces sialylation, while testosterone increases sialylation.
Journal of Endocrinology (1990) 125, 3–14
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Abstract
Experiments were done to study the effects of porcine relaxin on osmotically evoked changes in intramammary pressure and the release of oxytocin and vasopressin in anaesthetized rats. Injections (1 μ1) of hypertonic (0·75 m) NaCl into the left lateral cerebral ventricle were used to induce consistent rises in intramammary pressure and the release of oxytocin and vasopressin. Plasma hormone concentration was determined by radioimmunoassay. Relaxin (5 μg i.v.) significantly (P<0·05) suppressed the intramammary pressure response to osmotic challenge 5 and 10 min after treatment. However, pretreatment with a specific vasopressin V1 receptor antagonist completely negated the effect of relaxin on intramammary pressure. Baseline levels of oxytocin and vasopressin in unstimulated rats were 41 ± 1·6 and 36±1·1 pmol/l respectively. Osmotic challenge induced significant (P<0·05) rises in plasma levels of both hormones (62·8 ±1·1 and 67·9 ± 1·2 pmol/l respectively) which were further augmented by relaxin (81·3±1·8 and 117·1 ±2·4 pmol/l respectively; P<0·05). The data confirm that central osmotic challenge provokes the release of oxytocin and vasopressin but the effects of oxytocin at the level of the mammary gland may be obscured by the action of vasopressin affecting blood flow to the gland.
Journalof Endocrinology (1994) 141, 75–80
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ABSTRACT
The influence of various endocrine and environmental factors on pituitary-ovarian function was studied in peripubertal rats treated with pregnant mare serum gonadotrophin (PMSG). Pregnant mare serum gonadotrophin induced ovulation in rats aged 27 days provided they weighed over 60 g. The response was preceded by a marked hypersecretion of LH which was detectable by radioimmunological and biological assay methods. In contrast, smaller rats of the same age did not ovulate in response to PMSG apparently because of the secretion of a pleiomorphic form of LH which, although immunoreactive, appeared to be biologically inactive. Ovarian function, assessed by response to exogenous gonadotrophins and by measurement of 125I-labelled human chorionic gonadotrophin binding, was normal despite the presence of the biologically inactive pleiomorph. Exposure of the small PMSG-treated rats to a high environmental temperature (39 °C) or treatment with corticosterone or GH altered the nature of the LH in the blood so that it was active in both assay systems and facilitated ovulation as also did ACTH. The results suggest that the abrupt change in the nature of the LH released by the pituitary gland essential for the initiation of ovulation may be affected by GH, corticosterone or a raised environmental temperature.
J. Endocr. (1985) 104, 179–183
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Plasma concentrations of α-melanocyte-stimulating hormone (α-MSH) were measured by radioimmunoassay at various times during the oestrous cycle of the rat. Variations in plasma α-MSH concentrations occurred throughout the oestrous cycle. Plasma α-MSH concentrations were low during the day of dioestrus 1 and rose during the evening reaching peak levels at around 02.00 and 06.00 h on dioestrus 2. Plasma α-MSH concentrations then fell and remained low throughout the rest of dioestrus 2. A different pattern was observed during pro-oestrus and oestrus. On those days peak α-MSH concentrations occurred during the morning and persisted until the onset of the dark period at around 17.00 h.
Plasma α-MSH concentrations in ovariectomized rats were found to be increased 24 h after administration of a single injection of oestradiol benzoate and at 12 and 36 h after a single injection of progesterone. It is suggested that these ovarian steroids may influence the rhythm in plasma α-MSH concentration that occurs during the oestrous cycle.
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SUMMARY
The pattern of hormonal changes just before ovulation was investigated in immature rats induced to ovulate with pregnant mare serum gonadotrophin (PMSG). Oestradiol levels in the blood reached a maximum 42–52 h after PMSG treatment and then decreased dramatically. Pituitary luteinizing hormone (LH) levels remained constant until the time of the critical period (50–52 h) and then fell significantly. Plasma LH levels started to rise at 52 h, reached a peak at 54 h and fell to undetectable levels by 58 h. Plasma progesterone also reached a peak at 54 h and then fell slowly over the following dark period. The timing and pattern of changes in plasma and pituitary hormone levels were very similar to those seen in adult rats before ovulation. There was a positive correlation between the dose of PMSG, the peak concentration of plasma oestradiol and the average number of ova shed.
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ABSTRACT
The effect on ovulation of intraventricular infusions of noradrenaline, adrenaline and various pharmacological agents acting on the adrenergic receptor subtypes were investigated in cyclic female rats on the day of pro-oestrus. The inhibitory effects on ovulation of the different infusions were monitored by administering the drugs before 11.00 h (several hours before the critical period for the ovulatory LH surge). In experiments designed to show how the drugs under investigation might stimulate ovulation, pentobarbitone sodium (35 mg/kg) was given at 14.30 h; this anaesthetic inhibits ovulation and its effects can be overcome by substances that advance the preovulatory LH surge.
Noradrenaline (an α-agonist) stimulated ovulation when administered on the morning of pro-oestrus to rats injected with pentobarbitone early in the afternoon of the same day. Phenoxybenzamine and phentolamine (non-selective α-antagonists) and clonidine (a selective α2-agonist) all inhibited ovulation when infused on the morning of pro-oestrus. Yohimbine (a moderately selective α2-antagonist) neither stimulated nor inhibited ovulation.
Both isoprenaline (a non-selective β-agonist) and fenoterol (a selective β2-agonist) stimulated ovulation in pentobarbitone-treated rats when administered on the morning of pro-oestrus and fenoterol was also able to overcome the pentobarbitone block when infused later in the afternoon. Propranolol (a non-selective β-antagonist) and metoprolol (a selective β1-antagonist) were stimulatory only when administered in the afternoon.
Adrenaline (both an α- and β-agonist), prenalterol (a selective β1-agonist), atenolol (a selective β1-antagonist) and ICI 118, 551 (a selective β2-antagonist) neither stimulated nor inhibited ovulation.
The effect of intraventricular infusions of two selected β-adrenergic drugs was also investigated in ovariectomized rats primed with 2 μg oestradiol benzoate 48 h previously. Isoprenaline and fenoterol were able to stimulate LH release at 40 and 10 min respectively after their administration.
These results suggest a possible involvement of a stimulatory β2-adrenergic component in the neural regulation of the preovulatory LH surge along with the well-documented α-stimulatory component, which together may mask the possible inhibitory effects of a β1-adrenergic system.
J. Endocr. (1985) 106, 143–151
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ABSTRACT
The effects of castration with or without testosterone replacement in the adult male rat were studied to investigate possible hypothalamic mechanisms by which changes in gonadotrophin secretion occur at different times after castration, with particular reference to the continuing LH rise and its lack of suppression by testosterone in the long-term castrated rat. Castrated rats received either subcutaneous silicone elastomer implants containing testosterone or empty implants at the time of castration, and a sham-operated group served as controls.
At 1, 10 and 40 days after castration, there were six-, 15- and 25-fold rises respectively in LH and 1·5-, two-and fivefold rises in FSH. However, there were no significant changes in hypothalamic noradrenaline concentration and turnover or in α-adrenoceptor density and affinity at any time after castration. Testosterone implants were effective in suppressing gonadotrophin release at 1 and 10 days, but not at 40 days after castration, and did not significantly affect hypothalamic noradrenaline turnover or α-adrenoceptors at any time.
Neither acute inhibition of the noradrenergic system, using either the α-adrenoceptor blockers phenoxybenzamine and phentolamine or the synthesis inhibitor α-methyl-p-tyrosine, nor chronic depletion of hypothalamic noradrenaline by 6-hydroxydopamine had any significant effect on the normal rise in LH levels seen on days 10 and 40 after castration, and did not alter the ability of testosterone to suppress LH levels. This indicates that, in the long-term castrated rat, the noradrenergic system may not be involved in the control of gonadotrophin release. However, at 16 h after castration, α-adrenoceptor blockers and α-methyl-p-tyrosine did reduce LH levels, indicating that the noradrenergic system is likely to be involved in the short-term response to castration.
J. Endocr. (1984) 100, 235–244
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Measurements of the refractory period of stria terminalis neurones that are sensitive to testosterone propionate, of sexual behaviour and of plasma levels of LH were taken in castrated rats at various times after initiation of treatment with testosterone propionate. Levels of LH dropped within 24 h, before there was any change in neuronal refractory periods. The period of latency to mounting, however, was reduced to its shortest only after 7–8 days and ejaculations first occurred at the same time; these sexual responses correlated in time with the reduction of the neuronal refractory period to its lowest level.
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The concentrations of LH, progesterone, ACTH, corticosterone and thyroxine in the plasma were estimated at various times during the oestrous cycle of the rat. The well-established patterns of LH and progesterone secretion were confirmed. On each day of the cycle the plasma concentrations of ACTH and corticosterone were lowest in the morning and rose in the afternoon. Conversely, during oestrus and dioestrus, the plasma concentrations of thyroxine were higher in the morning than in the evening. However, during the afternoon of pro-oestrus the concentrations of ACTH, corticosterone and thyroxine in the plasma rose and, like the concentrations of LH and progesterone, all reached levels far higher than those attained at any other time of the cycle.
