scholarly journals Neuroendocrine Aging in the Female Rat: The Changing Relationship of Hypothalamic Gonadotropin-Releasing Hormone Neurons and N-Methyl-d-Aspartate Receptors**Preliminary versions of this work were presented at the 28th and 29th Annual Meetings of the Society for Neuroscience (Abstracts 110.11 and 777.10). This work was supported by the Brookdale Foundation (to A.C.G.), NIH Grant 1-PO1-AG16765–01 (to A.C.G. and J.H.M.).

Endocrinology ◽  
2000 ◽  
Vol 141 (12) ◽  
pp. 4757-4767 ◽  
Author(s):  
Andrea C. Gore ◽  
Glendy Yeung ◽  
John H. Morrison ◽  
Twethida Oung
Keyword(s):  
Critical Role ◽  
Reproductive Status ◽  
Female Rats ◽  
Mrna Levels ◽  
Female Rat ◽  
Messenger Rnas ◽  
Middle Aged ◽  
Medial Basal Hypothalamus ◽  
Aging Rats ◽  
Gnrh Neurons

Abstract The reproductive axis undergoes alterations during aging, resulting in acyclicity and the loss of reproductive function. In the hypothalamus, changes intrinsic to GnRH neurons may play a critical role in this process, as may changes in inputs to GnRH neurons from neurotransmitters such as glutamate. We investigated the effects of age and reproductive status on neuroendocrine glutamatergic NMDA receptors (NRs), their regulation of GnRH neurons, and their expression on GnRH neurons, in female rats. First, we quantified NR subunit messenger RNAs (mRNAs) in preoptic area-anterior hypothalamus (POA-AH) and medial basal hypothalamus (MBH), the sites of GnRH perikarya and neuroterminals, respectively. In POA-AH, NR1 mRNA levels varied little with age or reproductive status. NR2a and NR2b mRNA levels decreased significantly between cycling and acyclic rats. In MBH, NR mRNAs all increased with aging, particularly in acyclic animals. Second, we tested the effects of N-methyl-d,l-aspartate (NMA) on GnRH mRNA levels in POA-AH of aging rats. NMA elevated GnRH mRNA levels in young rats, but decreased them in middle-aged rats. Third, we quantified expression of the NR1 subunit on GnRH perikarya in aging rats using double label immunocytochemistry. NR1 expression on GnRH cell bodies varied with age and reproductive status, with 30%, 19%, and 46% of GnRH somata double labeled with NR1 in young proestrous, middle-aged proestrous, and middle-aged persistent estrous rats, respectively. Thus, 1) the expression of hypothalamic NR subunit mRNAs correlates with reproductive status; 2) changes in NR subunit mRNA levels, if reflected by changes in protein levels, may result in alterations in the stoichiometry of the NR during aging, with possible physiological consequences; 3) the effects of NR activation on GnRH mRNA switches from stimulatory to inhibitory during reproductive aging; and 4) expression of the NR1 subunit on GnRH perikarya changes with reproductive status. These molecular, physiological, and cellular neuroendocrine changes are proposed to be involved in the transition to acyclicity in aging female rats.

scholarly journals Vasoactive Intestinal Peptide Modulation of the Steroid-Induced LH Surge Involves Kisspeptin Signaling in Young but Not in Middle-Aged Female Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (6) ◽  
pp. 2222-2232 ◽  
Author(s):  
Alexander S. Kauffman ◽  
Yan Sun ◽  
Joshua Kim ◽  
Azim R. Khan ◽  
Jun Shu ◽  
...  
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Suprachiasmatic Nucleus ◽  
Reproductive Age ◽  
Female Rats ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Middle Aged ◽  
Lh Surge ◽  
Young Females ◽  
Gnrh Neurons

Age-related LH surge dysfunction in middle-aged rats is characterized, in part, by reduced responsiveness to estradiol (E2)-positive feedback and reduced hypothalamic kisspeptin neurotransmission. Vasoactive intestinal peptide (VIP) neurons in the suprachiasmatic nucleus project to hypothalamic regions that house kisspeptin neurons. Additionally, middle-age females express less VIP mRNA in the suprachiasmatic nucleus on the day of the LH surge and intracerebroventricular (icv) VIP infusion restores LH surges. We tested the hypothesis that icv infusion of VIP modulates the LH surge through effects on the kisspeptin and RFamide-related peptide-3 (RFRP-3; an estradiol-regulated inhibitor of GnRH neurons) neurotransmitter systems. Brains were collected for in situ hybridization analyses from ovariectomized and ovarian hormone-primed young and middle-aged females infused with VIP or saline. The percentage of GnRH and Kiss1 cells coexpressing cfos and total Kiss1 mRNA were reduced in saline-infused middle-aged compared with young females. In young females, VIP reduced the percentage of GnRH and Kiss1 cells coexpressing cfos, suggesting that increased VIP signaling in young females adversely affected the function of Kiss1 and GnRH neurons. In middle-aged females, VIP increased the percentage of GnRH but not Kiss1 neurons coexpressing cfos, suggesting VIP affects LH release in middle-aged females through kisspeptin-independent effects on GnRH neurons. Neither reproductive age nor VIP affected Rfrp cell number, Rfrp mRNA levels per cell, or coexpression of cfos in Rfrp cells. These data suggest that VIP differentially affects activation of GnRH and kisspeptin neurons of female rats in an age-dependent manner.

scholarly journals Hypothalamic Molecular Changes Underlying Natural Reproductive Senescence in the Female Rat

Endocrinology ◽  
2014 ◽  
Vol 155 (9) ◽  
pp. 3597-3609 ◽  
Author(s):  
Bailey A. Kermath ◽  
Penny D. Riha ◽  
Michael J. Woller ◽  
Andrew Wolfe ◽  
Andrea C. Gore
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Steroid Hormone Receptors ◽  
Female Rats ◽  
Mrna Levels ◽  
Female Rat ◽  
Aged Rats ◽  
Middle Aged ◽  
Reproductive Senescence ◽  
Periventricular Nucleus

Abstract The role of the hypothalamus in female reproductive senescence is unclear. Here we identified novel molecular neuroendocrine changes during the natural progression from regular reproductive cycles to acyclicity in middle-aged female rats, comparable with the perimenopausal progression in women. Expression of 48 neuroendocrine genes was quantified within three hypothalamic regions: the anteroventral periventricular nucleus, the site of steroid positive feedback onto GnRH neurons; the arcuate nucleus (ARC), the site of negative feedback and pulsatile GnRH release; and the median eminence (ME), the site of GnRH secretion. Surprisingly, the majority of changes occurred in the ARC and ME, with few effects in anteroventral periventricular nucleus. The overall pattern was increased mRNA levels with chronological age and decreases with reproductive cycle status in middle-aged rats. Affected genes included transcription factors (Stat5b, Arnt, Ahr), sex steroid hormone receptors (Esr1, Esr2, Pgr, Ar), steroidogenic enzymes (Sts, Hsd17b8), growth factors (Igf1, Tgfa), and neuropeptides (Kiss1, Tac2, Gnrh1). Bionetwork analysis revealed region-specific correlations between genes and hormones. Immunohistochemical analyses of kisspeptin and estrogen receptor-α in the ARC demonstrated age-related decreases in kisspeptin cell numbers as well as kisspeptin-estrogen receptor-α dual-labeled cells. Taken together, these results identify unexpectedly strong roles for the ME and ARC during reproductive decline and highlight fundamental differences between middle-aged rats with regular cycles and all other groups. Our data provide evidence of decreased excitatory stimulation and altered hormone feedback with aging and suggest novel neuroendocrine pathways that warrant future study. Furthermore, these changes may impact other neuroendocrine systems that undergo functional declines with age.

Effect of Fetal and Neonatal Hypothyroidism on Glucose Tolerance in Middle-Aged Female Rats

2020 ◽  
Vol 20 ◽  
Author(s):  
Sajad Jeddi ◽  
Saeedeh Khalifi ◽  
Mahboubeh Ghanbari ◽  
Asghar Ghasemi
Keyword(s):  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Female Offspring ◽  
Female Rats ◽  
Control Group ◽  
Female Rat ◽  
Middle Aged ◽  
Intravenous Glucose ◽  
Neonatal Hypothyroidism ◽  
Glucose Levels

Background and objective: The effects of hypothyroidism during pregnancy and lactation on carbohydrate metabolism have been mostly studied in male animals. The aim of this study is therefore to investigate effect of fetal and neonatal hypothyroidism (FH and NH) on the glucose tolerance in middle-aged female rat offspring. Methods: Pregnant female rats were divided into three groups: Rats in the control group consumed tap water, while those in the FH and NH groups consumed 250 mg/L of 6-propyl-2-thiouracil (PTU) in their drinking water during gestation or lactation periods, respectively. After weaning, the female offspring were separated and divided into 3 groups (n=8/group): Control, FH, and NH. Body weight was recorded monthly and intravenous glucose tolerance test (IVGTT) was performed at month 12. Results: Compared to controls, female rats in the FH group had significantly higher plasma glucose levels than controls throughout the IVGTT except at min 60. Values at min 5 of the FH and control group were 196.1±1.9 and 155.3±5.9 mg/dL, respectively (P<0.05). In the NH group, plasma glucose levels were significantly higher only at min 5 (185.7±14.1 vs. 155.3±5.9 mg/dL, P<0.05). Conclusion: Hypothyroidism during fetal or neonatal periods caused glucose intolerance in middle-aged female offspring rats.

Induction of growth hormone (GH) mRNA by pulsatile GH-releasing hormone in rats is pattern specific

2000 ◽  
Vol 278 (5) ◽  
pp. E885-E891 ◽  
Author(s):  
Russell J. Borski ◽  
Wellington Tsai ◽  
Roberta Demott-Friberg ◽  
Ariel L. Barkan
Keyword(s):  
Growth Hormone ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Somatic Growth ◽  
Pulse Amplitude ◽  
Female Rats ◽  
Mrna Levels ◽  
Female Rat ◽  
Constant Frequency ◽  
Releasing Hormone

Growth hormone-releasing hormone (GHRH) is a main inducer of growth hormone (GH) pulses in most species studied to date. There is no information regarding the pattern of GHRH secretion as a regulator of GH gene expression. We investigated the roles of the parameters of exogenous GHRH administration (frequency, amplitude, and total amount) upon induction of pituitary GH mRNA, GH content, and somatic growth in the female rat. Continuous GHRH infusions were ineffective in altering GH mRNA levels, GH stores, or weight gain. Changing GHRH pulse amplitude between 4, 8, and 16 μg/kg at a constant frequency (Q3.0 h) was only moderately effective in augmenting GH mRNA levels, whereas the 8 μg/kg and 16 μg/kg dosages stimulated weight gain by as much as 60%. When given at a 1.5-h frequency, GHRH doubled the amount of GH mRNA, elevated pituitary GH stores, and stimulated body weight gain. In the rat model, pulsatile but not continuous GHRH administration is effective in inducing pituitary GH mRNA and GH content as well as somatic growth. These studies suggest that the greater growth rate, pituitary mRNA levels, and GH stores seen in male compared with female rats are likely mediated, in part, by the endogenous episodic GHRH secretory pattern present in males.

Regulation of prolactin receptor gene expression by thyroid hormone status in the rat

1992 ◽  
Vol 8 (1) ◽  
pp. 63-72 ◽  
Author(s):  
T. S. Tiong ◽  
J. L. Stevenson ◽  
A. C. Herington
Keyword(s):  
Thyroid Hormone ◽  
Tissue Distribution ◽  
Prolactin Receptor ◽  
Combined Treatment ◽  
Female Rats ◽  
Male Rat ◽  
Mrna Levels ◽  
Female Rat ◽  
Thyroid Status ◽  
Mrna Species

ABSTRACT The nature and tissue distribution of prolactin receptor (PRL-R) mRNA in both male and female rats was studied. A single mRNA species of 2.2kb was identified in the liver, kidney, adrenal, prostate, lactating mammary gland and ovary but not in the male lung, heart, skeletal muscle, thymus, adipose tissue or brain. There were distinct and contrasting sex differences in abundance of PRL-R mRNA in some tissues: liver (female>>male), kidney and adrenal (male >>female). A mRNA species of 4kb was occasionally detected in the male adrenal and female liver. Given previous reports on the effects of thyroid status on PRL binding, the effects of thyroxine (T4), propylthiouracil (PTU) or combined treatment on PRL-R mRNA were assessed. In the male rat, PTU treatment markedly increased (three- to fourfold) PRL-R mRNA in the liver but decreased it (∼50%) in the kidney. These changes were reflected in similar changes in lactogenic binding activity. T4 or PTU treatment increased PRL-R mRNA in the prostate, with no obvious changes in binding. No major changes were seen in adrenal glands. In the female rat, PTU had little effect on PRL-R mRNA in any tissue, although binding of 125I-labelled lactogen was decreased in both the liver and kidney. There was an unexpected threefold rise in PRL-R mRNA in the female kidney following combined T4 and PTU treatment. Overall, there was a quite close correlation between the effects of thyroid status on PRL-R mRNA levels and specific lactogenic binding to membranes prepared from the same tissue samples. These studies provide data on the tissue distribution and size of PRL-R mRNA in rats and suggest a novel and complex tissue- and sex-dependent regulation by thyroid hormone.

scholarly journals Corticosteroid-binding globulin is a biomarker of inflammation onset and severity in female rats

2016 ◽  
Vol 230 (2) ◽  
pp. 215-225 ◽  
Author(s):  
Lesley A Hill ◽  
Tamara S Bodnar ◽  
Joanne Weinberg ◽  
Geoffrey L Hammond
Keyword(s):  
Critical Role ◽  
Clinical Signs ◽  
Experimental Period ◽  
Apparent Size ◽  
Binding Activity ◽  
Female Rats ◽  
Mrna Levels ◽  
Severe Inflammation ◽  
Corticosteroid Binding Globulin ◽  
And Function

Plasma corticosteroid-binding globulin (CBG) plays a critical role in regulating glucocorticoid bioavailability and is an acute phase ‘negative’ protein during inflammation. In an adjuvant-induced arthritis model, plasma CBG levels decrease in rats that develop severe inflammation, and we have now determined when and how these reductions in CBG occur. After administering complete Freund’s adjuvant or saline intra-dermally at the tail base, blood samples were taken periodically for 16days. In adjuvant-treated rats, decreases in plasma CBG levels matched the severity of inflammation, and decreases were observed 4days before any clinical signs of inflammation. Decreases in CBG levels coincided with an ~5kDa reduction in its apparent size, consistent with proteolytic cleavage, and cleaved CBG lacked steroid-binding activity. At the termination of the experimental period, hepatic Cbg mRNA levels were decreased in rats with severe inflammation. While plasma TNF-α increased in all adjuvant-treated rats, increases in Il-4, IL-6, IL-10, IL-13 and IFN-γ were only observed in rats with cleaved CBG. Rats with cleaved CBG also exhibited increased spleen weights, and strong negative correlations were observed among CBG, IL-6 and spleen weights, respectively. However, there were no differences in hepatic Cbg mRNA levels in relation to the apparent proteolysis of CBG, suggesting that CBG cleavage occurs before changes in hepatic Cbg expression. Our results indicate that the levels and integrity of plasma CBG are biomarkers of the onset and severity of inflammation. Dynamic changes in the levels and function of CBG likely modulate the tissue availability of corticosterone during inflammation.

scholarly journals Prenatal androgen excess enhances stimulation of the GNRH pulse in pubertal female rats

2014 ◽  
Vol 222 (1) ◽  
pp. 73-85 ◽  
Author(s):  
Xiaonan Yan ◽  
Chun Yuan ◽  
Nannan Zhao ◽  
Yugui Cui ◽  
Jiayin Liu
Keyword(s):  
Polycystic Ovary ◽  
Elevated Serum ◽  
Pulse Frequency ◽  
Female Rats ◽  
Mrna Levels ◽  
Pregnant Rats ◽  
Serum Lh ◽  
Gnrh Neurons ◽  
Prenatal Androgen ◽  
Stimulation Of

In adolescent girls with polycystic ovary syndrome (PCOS), neuroendocrine derangements manifest after the onset of puberty, characterized by rapid LH pulse frequency. The early mechanism underlying the pubertal regulation of the GNRH/LH pulsatile release in adolescents with PCOS remains uncertain. To determine the effects of prenatal androgen exposure on the activation of GNRH neurons and generation of LH pulse at puberty, we administrated 5α-dihydrotestosterone to pregnant rats and observed serum LH levels and expression of hypothalamic genes in female offspring from postnatal 4 to 8 weeks. The 6-week-old prenatally androgenized (PNA) female rats exhibited an increase in LH pulse frequency. The hypothalamic expression of neurokinin B (Nkb(Tac2)) andLeprmRNA levels in PNA rats increased remarkably before puberty and remained high during puberty, whereas elevatedKiss1mRNA levels were detected only after the onset of puberty. Exogenous kisspeptin, NK3R agonist, and leptin triggered tonic stimulation of GNRH neurons and increased LH secretion in 6-week-old PNA rats. Leptin upregulatedKiss1mRNA levels in the hypothalamus of pubertal PNA rats; however, pretreatment with a kisspeptin antagonist failed to suppress the elevated serum LH stimulated by leptin, indicating that the stimulatory effects of leptin may be conveyed indirectly to GNRH neurons via other neural components within the GNRH neuronal network, rather than through the kisspeptin–GPR54 pathway. These findings validate the hypotheses that NKB and leptin play an essential role in the activation of GNRH neurons and initiation of increased LH pulse frequency in PNA female rats at puberty and that kisspeptin may coordinate their stimulatory effects on LH release.

Estrogen potentiates constrictor prostanoid function in female rat aorta by upregulation of cyclooxygenase-2 and thromboxane pathway expression

2008 ◽  
Vol 294 (6) ◽  
pp. H2444-H2455 ◽  
Author(s):  
Min Li ◽  
Lih Kuo ◽  
John N. Stallone
Keyword(s):  
Vascular Reactivity ◽  
Molecular Mechanisms ◽  
Rat Aorta ◽  
Arachidonic Acid Metabolism ◽  
Female Rats ◽  
Mrna Levels ◽  
Female Rat ◽  
Pathway Expression ◽  
Cox 2 ◽  
Cox 1

Estrogen potentiates vascular reactivity to vasopressin (VP) by enhancing constrictor prostanoid function. To determine the cellular and molecular mechanisms, the effects of estrogen on arachidonic acid metabolism and on the expression of constrictor prostanoid pathway enzymes and endoperoxide/thromboxane receptor (TP) were determined in the female rat aorta. The release of thromboxane A2 (TxA2) and prostacyclin (PGI2) was measured in male (M), intact-female (Int-F), ovariectomized-female (OvX-F), and OvX + 17β-estradiol-replaced female (OvX + ER-F) rats. The expression of mRNA for cyclooxygenase (COX)-1, COX-2, thromboxane synthase (TxS), and TP by aortic endothelium (Endo) and vascular smooth muscle (VSM) of these four experimental groups was measured by RT-PCR. The expression of COX-1, COX-2, and TxS proteins by Endo and VSM was also estimated by immunohistochemistry (IHC). Basal release of TxA2 and PGI2 was similar in M (18.8 ± 1.9 and 1,723 ± 153 pg/mg ring wt/45 min, respectively) and Int-F (20.2 ± 4.2 and 1,488 ± 123 pg, respectively) rat aortas. VP stimulated the dose-dependent release of TxA2 and PGI2 from both male and female rat aorta. OvX markedly attenuated and ER therapy restored VP-stimulated release of TxA2 and PGI2 in female rats. No differences in COX-1 mRNA levels were detected in either Endo or VSM of the four experimental groups ( P > 0.1). The expression of both COX-2 and TxS mRNA were significantly higher ( P < 0.05) in both Endo and VSM of Int-F and OvX + ER-F, compared with M or OvX-F. Expression of TP mRNA was significantly higher in VSM of Int-F and OvX + ER-F compared with M or OvX-F. IHC revealed the uniform staining of COX-1 in VSM of the four experimental groups, whereas staining of COX-2 and TxS was greater in Endo and VSM of Int-F and OvX + ER-F than in OvX-F or M rats. These data reveal that estrogen enhances constrictor prostanoid function in female rat aorta by upregulating the expression of COX-2 and TxS in both Endo and VSM and by upregulating the expression of TP in VSM.

Pup contact induces the expression of long form prolactin receptor mRNA in the brain of female rats: effects of ovariectomy and hypophysectomy on receptor gene expression

1996 ◽  
Vol 149 (2) ◽  
pp. 335-340 ◽  
Author(s):  
T Sugiyama ◽  
H Minoura ◽  
N Toyoda ◽  
K Sakaguchi ◽  
M Tanaka ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Choroid Plexus ◽  
Prolactin Receptor ◽  
Female Rats ◽  
Maternal Behaviour ◽  
Mrna Levels ◽  
Female Rat ◽  
Expression Levels ◽  
Long Form ◽  
The Brain

Abstract Prolactin receptor (PRL-R) mRNA expression levels in the female rat brain (cerebrum) during pup contact stimulation were determined by the reverse transcription-PCR method. The high expression levels of long form PRL-R mRNA found in the brain of lactating rats were markedly reduced by removal of pups, and long form PRL-R mRNA levels were recovered by resumption of pup contact. Interestingly, pup contact stimuli of nulliparous virgin rats also markedly induced long form but not short form PRL-R mRNA expression in the brain in 1·3 days, together with the expression of maternal behaviour. In ovariectomized (OVX) or hypophysectomized (HYPOX) virgin rats, or in OVX plus HYPOX virgin rats, however, brain long form PRL-R mRNA was not significantly induced by pup contact stimuli for as long as 7 days, while maternal behaviour was fully expressed in these rats after 7 days of pup contact. The in situ hybridization experiments revealed that the long form PRL-R mRNA induced in virgin rats in contact with pups or in lactating rats was localized in the epithelial cells of the choroid plexus. No significant increase in mRNA was detected in other regions of the brain, such as the hypothalamus or cortex, in these maternal female rats. These results suggest that pup contact induces the expression of long form PRL-R mRNA in the choroid plexus of the brain in the presence of female sex steroid and pituitary hormones for the rapid expression of maternal behaviour. Our studies also suggested that maternal behaviour can be expressed in OVX or HYPOX rats after exposure to pups for 7 days without any significant increase in brain PRL-R mRNA expression. Journal of Endocrinology (1996) 149, 335–340

scholarly journals Hypothalamic Expression of Eap1 Is Not Directly Controlled by Ovarian Steroids

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1870-1878 ◽  
Author(s):  
Valerie Matagne ◽  
Claudio Mastronardi ◽  
Robert A. Shapiro ◽  
Daniel M. Dorsa ◽  
Sergio R. Ojeda
Keyword(s):  
Preoptic Area ◽  
In Vitro Assays ◽  
Mrna Levels ◽  
Female Rat ◽  
Juvenile Period ◽  
Medial Basal Hypothalamus ◽  
Ovarian Steroids ◽  
Estrogen Responsive Element ◽  
General Decline ◽  
Responsive Element

A gene termed EAP1 (enhanced at puberty 1) was recently identified as a transcriptional regulator of female neuroendocrine reproductive function. We have now used in vivo and in vitro assays, and the female rat as an animal model, to determine whether Eap1 gene expression is regulated by ovarian steroids. Eap1 mRNA abundance decreases in both the hypothalamus and cerebral cortex during the infantile-juvenile phases of development, but it increases selectively in the hypothalamus at puberty, suggesting that in contrast to the general decline in expression observed in immature animals, the region-specific increase in Eap1 mRNA levels that occurs at puberty might be elicited by ovarian steroids. This is, however, not the case, because hypothalamic Eap1 mRNA levels increase at the expected time of puberty in rats ovariectomized at the beginning of the juvenile period. Although a subpopulation of EAP1-containing cells in the medial basal hypothalamus (MBH) and preoptic area express estrogen receptor-α (ERα), the 5′-flanking region of the rat Eap1 (rEap1) gene does not contain a complete estrogen-responsive element, and no such estrogen-responsive element is detected within 100 kb of the rEap1 locus. Functional promoter assays showed that neither estradiol (E2) alone nor a combination of E2 plus progesterone increases rEap1 gene transcription. Likewise, E2 administered to ovariectomized immature rats elicited a robust surge of LH but increased neither preoptic area nor MBH Eap1 mRNA levels. E2/progesterone-treated rats showed a massive elevation in plasma LH but only a modest increase in Eap1 mRNA levels, limited to the MBH. These results indicate that hypothalamic Eap1 expression is not directly controlled by ovarian steroids and suggest that Eap1 expression increases at puberty driven by ovary-independent, centrally initiated events.

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