Ovarian steroids normally exert homeostatic negative feedback on GnRH release. During sustained exposure to elevated estradiol in the late follicular phase of the reproductive cycle, however, the feedback action of estradiol switches to positive, inducing a surge of GnRH release from the brain, which signals the pituitary LH surge that triggers ovulation. In rodents, this switch appears dependent on a circadian signal that times the surge to a specific time of day (e.g., late afternoon in nocturnal species). Although the precise nature of this daily signal and the mechanism of the switch from negative to positive feedback have remained elusive, work in the past decade has provided much insight into the role of circadian/diurnal and estradiol-dependent signals in GnRH/LH surge regulation and timing. Here we review the current knowledge of the neurobiology of the GnRH surge, in particular the actions of estradiol on GnRH neurons and their synaptic afferents, the regulation of GnRH neurons by fast synaptic transmission mediated by the neurotransmitters γ-aminobutyric acid and glutamate, and the host of excitatory and inhibitory neuromodulators including kisspeptin, vasoactive intestinal polypeptide, catecholamines, neurokinin B, and RFamide-related peptides, that appear essential for GnRH surge regulation, and ultimately ovulation and fertility.

/pdf/the-neurobiology-of-preovulatory-and-estradiol-induced-3acffq75zj.pdf

The neurobiology of preovulatory and estradiol-induced gonadotropin-releasing hormone surges.

Neuroendocrine regulation of GnRH release in induced ovulators.

When doses of progestin used commercially are administered to synchronize the stage of the estrous cycle among bovine females, fertility is reduced compared with that of untreated controls. The reduced fertility that results from the use of progestin based estrus synchrony regimens is associated with the development of persistent ovarian follicles. Persistent ovarian follicles develop as a result of the greater frequency of LH pulses that occurs during the period of treatment with progestins. The greater release of LH pulses results in enhanced secretion of 17 beta-estradiol from persistent ovarian follicles. The greater frequency of LH release or the greater secretion of 17 beta-estradiol associated with development of persistent ovarian follicles probably contributes to the reduced fertility that occurs when progestins are used to synchronize stage of the estrous cycle.

/pdf/progestin-and-estrogen-regulation-of-pulsatile-lh-release-3cx3maej22.pdf

Progestin and estrogen regulation of pulsatile LH release and development of persistent ovarian follicles in cattle

GnRH signaling, the gonadotrope and endocrine control of fertility.

Timed artificial insemination (TAI) is a very important tool in production systems, as it has a direct impact on cost-efficiency by reducing labour resulting from oestrus detection. However, to make TAI commercially feasible, hormonal treatments need to assure acceptable pregnancy rates and be economically viable. Recent advances in the knowledge of ovarian physiology (e.g. determination of follicular waves, sensitivity of the early corpus luteum) in small ruminants allowed the development of new treatments focused on an efficient estimation and synchronisation of the time of ovulation of the females of a treated flock/herd. In this review we summarise new information and concepts in the hormonal control of the life span of the corpus luteum, as well as methods to manipulate follicular growth in small ruminants. Additionally, we elaborate on recent studies concerning the use of TAI associated with short progestogen treatment in goats and the newly developed Synchrovine protocol (two doses of prostaglandin F(2alpha) given seven days apart) in sheep.

New treatments associated with timed artificial insemination in small ruminants.

GnRH-receptor interaction. V. Down-regulation of pituitary receptors for GnRH in ovariectomized ewes by infusion of homologous hormone.

The effects of estradiol and progesterone on 1) hypophyseal and serum concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH); 2) hypothalamic content of gonadotropin releasing hormone (GnRH); and 3) numbers of receptors for GnRH were examined in ovariectomized ewes. Three days after ovariectomy, ewes were given 16 mg progesterone (n 5), 0.7 mg estradiol (n 5) or 16 mg progesterone plus 0.7 mg estradiol (n 5) s.c. in ethanol twice daily for 3 weeks prior to slaughter. Ten control ewes were given injections of ethanol according to the same schedule. Five intact ewes were killed 12 days after an induced ovulation. Blood samples were collected daily for 4 days prior to slaughter, and the serum was analyzed for concentrations of progesterone, estradiol, LH, and FSH. Hypothalami were removed after sacrifice and the amount of GnRH present in the preoptic area, median eminence, and hypothalamus proper was determined. In addition, the pituitary gland from each animal was removed and the number of receptors for GnRH and concentrations of LH, FSH, and prolactin were measured. Steroid treatment produced concentrations of estradiol and progesterone similar to those observed during late pregnancy in ewes. Administration of either progesterone or estradiol, suppressed (P 0.05) as a result of treatment. Likewise, neither hypophyseal weight nor prolactin content was affected by steroid treatment, suggesting that the effects of the steroids were limited to the gonadotrophs. These data indicate that estradiol can increase the number of receptors for GnRH, while the quantity of LH and FSH released into the circulation or contained in the pituitary decreases. Thus, the effects of estradiol appear to be mediated at the level of the pituitary gland. In contrast, the inhibitory effect of progesterone on secretion of LH is not mediated via receptors for GnRH or pituitary concentrations of LH, suggesting an influence at higher neural centers.

/pdf/gnrh-receptor-interaction-vi-effect-of-progesterone-and-4vqo7h8fcx.pdf

GnRH-Receptor Interaction. VI. Effect of Progesterone and Estradiol on Hypophyseal Receptors for GnRH, and Serum and Hypophyseal Concentrations of Gonadotropins in Ovariectomized Ewes

Acute changes of bovine pituitary luteinizing hormone-releasing hormone (LHRH) receptors in response to steroid challenges have not been documented. To investigate these changes 96 ovariectomized (OVX) cows were randomly allotted to one of the following treatments: 1) 1 mg estriol (E3); 2)1 mg 17j3-estradiol (E2); or 3) 25 mg progesterone (P) twice daily for 7 days before 1mg E2 and continuing to the end of the experiment Serum was collected at hourly intervals from 4 animals in each group for 28 h following estrogen treatment Four animals from each treatment were killed at 4-h intervals from 0 to 28 h after estrogen injection to recover pituitaries and hypethalami. Treatment with E3 or E3 decreased serum luteinizing hormone (LH) within 3 h and was followed by surges of LH that were temporally and quantitatively similar (P>O.05). Progesterone did not block the decline in serum LH, but did prevent (P 0.05) the pituitary gonadotropin increase. Concentrations of LHRH in the hypothalamus were similar (P>0.05) among treatments. Pituitary concentrations of receptors for LHRH were maximal (P<0.005) 12 h after estrogen injection (approximately 8 h before the LH surge), even in the presence of P. This study demonstrated that in the OVX cow: 1) E2 and E3 increased the concentration of receptors for LHRH and this increase occurred before the surge of LH; and 2) P did not block the E3-induced increase in pituitary receptors for LHRH but did prevent the surge of LH.

/pdf/pituitary-luteinizing-hormone-releasing-hormone-receptors-in-pupwzxf9r6.pdf

Pituitary luteinizing hormone-releasing hormone receptors in ovariectomized cows after challenge with ovarian steroids.

Ovariectomized (OVX), hypothalamo/pituitary-disconnected (HPD) ewes were used to ascertain the short-term effects of estradiol on the number of gonadotropin-releasing hormone (GnRH) receptors in the pituitary gland. The time course of the study was such that measurements were made during the period of short-term negative feedback and positive feedback. Groups of 4 OVX-HPD ewes were given 250-ng pulses of GnRH each hour and an i.m. injection of oil (Group 1) or 50 micrograms estradiol benzoate in oil (Groups 2-4). Blood samples were collected from each ewe prior to treatment with estradiol or oil and again immediately before slaughter. Groups 2, 3, and 4 were killed 6, 16, and 20 h, respectively, after administration of estradiol. Amplitudes of luteinizing hormone (LH) pulses and average plasma concentrations of LH were reduced 6 h after estradiol treatment. Sixteen and 20 h after injection, the average plasma LH levels were elevated, but pulse amplitudes were similar to preinjection values. The number of GnRH receptors was significantly (p less than 0.01) increased within 6 h of estrogen treatment and further increased 16 and 20 h after treatment. Pituitary content of LH was similar in all groups. These data indicate that the number of GnRH receptors in the pituitary gland of ewes can be acutely influenced by a direct effect of estradiol. However, the magnitude and direction of the change in receptors number does not account for the changes in pituitary responsiveness to GnRH, suggesting estradiol also modifies post-receptor mechanisms that influence secretion of LH.

Pituitary receptors for gonadotropin-releasing hormone in relation to changes in pituitary and plasma gonadotropins in ovariectomized hypothalamo/pituitary-disconnected ewes. II. A marked rise in receptor number during the acute feedback effects of estradiol.

Pituitary content of gonadotropins and GnRH-receptors in pregnant, postpartum and steroid-treated OVX ewes.

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