A Subgroup of LHRH Neurons in Guinea Pigs with Progestin Receptors Is Centrally Positioned within the Total Population of LHRH Neurons

King, Joan C.; Tai, Deborah W.; Hanna, Iris K.; Pfeiffer, Andreas F. H.; Haas, Peter; Ronsheim, Paul M.; Mitchell, Scott C.; Turcotte, Joanne C.; Blaustein, Jeffrey D.

doi:10.1159/000126848

Cited by 60 publications

(27 citation statements)

References 37 publications

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“…Which (if any) of these progesterone-receptive neurons are involved in the inhibitory effects of progesterone on the generation of the GnRH surge and whether they lie within, or impinge upon, the estradiol signal transmission pathway, however, remains to be elucidated. As stated above, although the majority of reports have been unable to locate progesterone receptors within GnRH neurons, it is worthy of note that one group, working in the guinea pig, has consistently found progesterone receptors in a small subpopulation (10%) of GnRH neurons (29), the physiological role of which is unknown. The existence of a similar subpopulation of progesterone receptive GnRH neurons, in the ewe, cannot be ruled out.…”

Section: Discussionmentioning

confidence: 99%

Progesterone Can Block Transmission of the Estradiol-Induced Signal for Luteinizing Hormone Surge Generation during a Specific Period of Time Immediately after Activation of the Gonadotropin-Releasing Hormone Surge-Generating System

Harris¹

1999

Endocrinology

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The preovulatory GnRH/LH surge in the ewe is stimulated by a rise in the circulating estradiol concentration that occurs in conjunction with preovulatory ovarian follicle development. In the presence of high levels of progesterone, such as during the luteal phase of the estrous/menstrual cycle, the stimulatory effects of elevated estradiol on GnRH/LH secretion are blocked. Recent work in the ewe has shown that a relatively short period of estradiol exposure can stimulate a GnRH/LH surge that begins after estrogenic support has been removed. This result suggests that surge generation is characterized by an estradiol-dependent period (during which the signal is read) and an estradiol-independent period (during which a cascade of neuronal events transmits the stimulatory signal to the GnRH neurosecretory system, which releases a surge of GnRH). In this series of studies, we addressed the hypothesis that progesterone can block transmission of the stimulatory estradiol signal after it has been read. Nine ovariectomized ewes were run through repeated artificial estrous cycles by sequential addition and removal of exogenous steroids. In study one, ewes received three treatments in a randomized cross-over design. Exposure to a follicular phase estradiol concentration for 10 h (positive control treatment) stimulated an LH surge in all ewes, as determined in hourly jugular blood samples. Maintenance of luteal phase progesterone concentrations throughout the artificial follicular phase (2 ϫ CIDR-G devices, negative control) blocked the stimulatory effects of a 10-h estradiol signal, and no ewes that received this treatment expressed an LH surge. In the experimental group, exposure to luteal phase levels of progesterone, during the period after the surge generating system had been activated by estradiol, blocked the LH surge in six of nine ewes. This result demonstrates that progesterone can block the surge, even when applied after the surge-generating system has been activated and, therefore, that it inhibits either the transmission of the estradiol signal and/or the release of the GnRH/LH surge. In study 2, we assessed whether sensitivity to the inhibitory effects of progesterone was confined to a specific stage of the transmission of the estradiol signal. Eight ewes were exposed to four treatments, over successive artificial estrous cycles. Positive and negative controls were similar to those described in Study 1, except the duration of the stimulatory estradiol signal was reduced to 8 h. The two experimental groups consisted of an EARLY P (progesterone) treatment, in which progesterone was given from hours 8 -13 after estradiol insertion (immediately after estradiol removal), and a LATE P treatment, in which progesterone was given from hours 13-18 (immediately before LH surge secretion). As expected, LH surges were stimulated and blocked, in response to the positive and negative controls, respectively. Whereas the EARLY P treatment blocked the LH surge in seven of eight ewes, the LATE P treatment was only succes...

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Section: Discussionmentioning

confidence: 99%

Progesterone Can Block Transmission of the Estradiol-Induced Signal for Luteinizing Hormone Surge Generation during a Specific Period of Time Immediately after Activation of the Gonadotropin-Releasing Hormone Surge-Generating System

Harris¹

1999

Endocrinology

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“…Previous observations on the morphology [42, 43, 44], the cellular location of steroid receptors [45], or immunocytochemical distribution [3, 46, 47]suggest the presence of distinct populations of GnRH-like cells in the brain of several mammals. However, location of HypGnRH and GnRH in distinct neuronal populations appears unlikely, since both peptides and their respective intermediate precursor forms are synthesized and released [7]by the neuronal GT1 cell line [48].…”

Section: Discussionmentioning

confidence: 99%

In vitro Secretion of Gonadotropin-Releasing Hormone (GnRH) and [Hydroxyproline<sup>9</sup>]GnRH from the Rat Hypothalamus Exhibits a Differential Sensitivity to Castration and Second Messengers

Rochdi¹,

Theraulaz²,

Enjalbert³

et al. 1998

Neuroendocrinology

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The decapeptide [hydroxyproline⁹]GnRH (HypGnRH) has been characterized as an endogenous posttranslational product of the gonadotropin-releasing hormone (GnRH) precursor in a wide range of mammalian brains. Despite consistent biological effects, its secretion by the hypothalamus remains hypothetical. We report here in vitro secretion of HypGnRH and GnRH by the hypothalamus from intact and castrated male rats and provide evidence that they are differentially regulated. Both peptides were identified by two anti-GnRH antibodies of different specificities after separation under two high-performance liquid chromatography conditions. Calcium dependency of HypGnRH release was demonstrated under stimulation with KCl in the absence or presence of Ca²⁺, as well as with Bay K 8644, veratridine, methoxyverapamil, or tetrodotoxin. Activation of signaling pathways involving adenylate cyclase and protein kinases A and C (PKC) induced HypGnRH release. Expression of data as percentage of release over tissue stores revealed a two- to threefold higher release of HypGnRH than of GnRH under the different modes of stimulation used, except under PKC activation which triggered a comparable recruitment of both peptides. Castration selectively affected PKC-coupled GnRH secretion which showed a twofold lesser release than in intact rats, while the HypGnRH release was unaffected. We conclude that HypGnRH and GnRH are not secreted from the hypothalamus according to the same mechanisms.

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“…Several experiments, including electrochemical stimulation (Everett et al, 1964) and deafferentation or lesion studies (Samson and McCann, 1979;Wise et al, 1981;Kalra and Kalra, 1983), have demonstrated that this is an important region for the induction of an LH surge and ovulation. Other studies have suggested that there may exist a primary subpopulation of GnRH neurons localized in this same region that is crucial for producing higher levels of GnRH in times of greater demand, e.g., the LH surge (Rubin et al, 1994;King et al, 1995). This subpopulation of GnRH neurons may be under developmental regulation, and it is quite possible that those neurons that express the NMDA receptor represent a phenotypically distinct subpopulation of GnRH neu- …”

Section: Discussionmentioning

confidence: 99%

Gonadotropin-Releasing Hormone and NMDA Receptor Gene Expression and Colocalization Change during Puberty in Female Rats

et al. 1996

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During development, an increase in gonadotropin-releasing hormone (GnRH) release occurs that is critical for the initiation of puberty. This increase is attributable, at least in part, to activation of the GnRH neurosecretory system by inputs from neurotransmitters, such as glutamate, acting via NMDA receptors. We examined changes in GnRH and NMDA-R1 gene expression by RNase protection assay of preoptic area-anterior hypothalamic (POA-AH) dissections of female rats undergoing normal puberty or in which precocious puberty was induced by treatment with the glutamate agonist NMA. GnRH mRNA levels increased significantly throughout normal development; this was accelerated by treatment with NMA. NMDA-R1 mRNA levels increased only between P10 and P20. The acceleration of the elevation in GnRH mRNA levels by NMDA suggests that a stimulation of GnRH gene expression may be a rate-limiting factor for the onset of puberty. This is attributable to a posttranscriptional mechanism because GnRH primary transcript levels, an index of proGnRH gene transcription, were not observed to change during puberty. Alterations in the colocalization of GnRH neurons with the NMDA-R1 subunit during puberty also were assessed immunocytochemically. The percentage of GnRH neurons that double-labeled with NMDA-R1 was 2% in prepubertal rats and 3% in pubertal rats; this increased to 19% in postpubertal rats. Taken together, these studies suggest that an increase in glutamatergic input to GnRH neurons plays a role in the increase in GnRH release and gene expression that occurs at the initiation of puberty.

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A Subgroup of LHRH Neurons in Guinea Pigs with Progestin Receptors Is Centrally Positioned within the Total Population of LHRH Neurons

Cited by 60 publications

References 37 publications

Progesterone Can Block Transmission of the Estradiol-Induced Signal for Luteinizing Hormone Surge Generation during a Specific Period of Time Immediately after Activation of the Gonadotropin-Releasing Hormone Surge-Generating System

Progesterone Can Block Transmission of the Estradiol-Induced Signal for Luteinizing Hormone Surge Generation during a Specific Period of Time Immediately after Activation of the Gonadotropin-Releasing Hormone Surge-Generating System

In vitro Secretion of Gonadotropin-Releasing Hormone (GnRH) and [Hydroxyproline<sup>9</sup>]GnRH from the Rat Hypothalamus Exhibits a Differential Sensitivity to Castration and Second Messengers

Gonadotropin-Releasing Hormone and NMDA Receptor Gene Expression and Colocalization Change during Puberty in Female Rats

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