scholarly journals Developmental Changes in GnRH Release in Response to Kisspeptin Agonist and Antagonist in Female Rhesus Monkeys (Macaca mulatta): Implication for the Mechanism of Puberty

Endocrinology ◽  
2012 ◽  
Vol 153 (2) ◽  
pp. 825-836 ◽  
Author(s):  
Kathryn A. Guerriero ◽  
Kim L. Keen ◽  
Robert P. Millar ◽  
Ei Terasawa
Keyword(s):  
Rhesus Monkeys ◽  
Developmental Stages ◽  
Developmental Changes ◽  
Partial Recovery ◽  
Ovarian Steroid ◽  
Medial Basal Hypothalamus ◽  
Female Rhesus ◽  
Gnrh Release ◽  
Agonist And Antagonist

Kisspeptin (KP) and KP-1 receptor (KISS1R) have emerged as important upstream regulators in the control of puberty. However, how developmental changes in KP-KISS1R contribute to the pubertal increase in GnRH release still remains elusive. In this study, we examined the effects of the KP agonist, human KP-10 (hKP-10), and the KP antagonist, peptide 234, on in vivo GnRH release in prepubertal and pubertal ovarian-intact female rhesus monkeys using a microdialysis method. We found that direct infusion of hKP-10 into the medial basal hypothalamus and stalk-median eminence region stimulated GnRH release in a dose-responsive manner, whereas infusion of peptide 234 suppressed GnRH release in both developmental stages. Because ovarian steroid feedback on GnRH release becomes prominent after the initiation of puberty in primates, we further examined whether ovarian steroids modify the GnRH response to hKP-10. Results demonstrate that the hKP-10-induced stimulation of GnRH release was eliminated by ovariectomy in pubertal, but not prepubertal, monkeys. Furthermore, replacement of estradiol into ovariectomized pubertal monkeys resulted in a partial recovery of the hKP-10-induced GnRH release. Collectively, these results suggest that a KISS1R-mediated mechanism, in addition to the pubertal increase in KP-54 release we previously reported, contributes to the pubertal increase in GnRH release and that there is a switch from an ovarian steroid-independent to -dependent mechanism in the response of GnRH to KP.

scholarly journals Developmental Increase in Kisspeptin-54 Release in Vivo Is Independent of the Pubertal Increase in Estradiol in Female Rhesus Monkeys (Macaca mulatta)

Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 1887-1897 ◽  
Author(s):  
Kathryn A. Guerriero ◽  
Kim L. Keen ◽  
Ei Terasawa
Keyword(s):  
Rhesus Monkeys ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Release Pattern ◽  
Female Rhesus ◽  
Gnrh Release ◽  
Important Regulator ◽  
Nocturnal Increase

Kisspeptin (KP) signaling has been proposed as an important regulator in the mechanism of puberty. In this study, to determine the role of KP in puberty, we assessed the in vivo release pattern of KP-54 from the basal hypothalamus/stalk-median eminence in prepubertal and pubertal ovarian-intact female rhesus monkeys. We found that there was a developmental increase in mean KP-54 release, pulse frequency, and pulse amplitude, which is parallel to the developmental changes in GnRH release that we previously reported. Moreover, a nocturnal increase in KP-54 release becomes prominent after the onset of puberty. Because the pubertal increase in GnRH release occurs independent of the pubertal increase in circulating gonadal steroids, we further examined whether ovariectomy (OVX) modifies the release pattern of KP-54. Results show that OVX in pubertal monkeys enhanced mean KP-54 release and pulse amplitude but not pulse frequency, whereas OVX did not alter the release pattern of KP-54 in prepubertal monkeys. Estradiol replacement in OVX pubertal monkeys suppressed mean KP-54 release and pulse amplitude but not pulse frequency. Estradiol replacement in OVX prepubertal monkeys did not alter the KP-54 release pattern. Collectively these results suggest that the pubertal increase in KP release occurs independent of the pubertal increase in circulating estradiol. Nevertheless, the pubertal increase in KP release is not likely responsible for the initiation of the pubertal increase in GnRH release. Rather, after puberty onset, the increase in KP release contributes to further increase GnRH release during the progression of puberty.

scholarly journals An increase in in vivo release of LHRH and precocious puberty by posterior hypothalamic lesions in female rhesus monkeys (Macaca mulatta)

2007 ◽  
Vol 292 (4) ◽  
pp. E1000-E1009 ◽  
Author(s):  
Bret M. Windsor-Engnell ◽  
Etsuko Kasuya ◽  
Masaharu Mizuno ◽  
Kim L. Keen ◽  
Ei Terasawa
Keyword(s):  
Precocious Puberty ◽  
Rhesus Monkeys ◽  
Gaba Release ◽  
Good Tool ◽  
Subsequent Increase ◽  
Female Rhesus ◽  
Before And After ◽  
Lhrh Release

We have previously shown that a decrease in γ-aminobutyric acid (GABA) tone and a subsequent increase in glutamatergic tone occur in association with the pubertal increase in luteinizing hormone releasing hormone (LHRH) release in primates. To further determine the causal relationship between developmental changes in GABA and glutamate levels and the pubertal increase in LHRH release, we examined monkeys with precocious puberty induced by lesions in the posterior hypothalamus (PH). Six prepubertal female rhesus monkeys (17.4 ± 0.1 mo of age) received lesions in the PH, three prepubertal females (17.5 ± 0.1 mo) received sham lesions, and two females received no treatments. LHRH, GABA, and glutamate levels in the stalk-median eminence before and after lesions were assessed over two 6-h periods (0600–1200 and 1800–2400) using push-pull perfusion. Monkeys with PH lesions exhibited external signs of precocious puberty, including significantly earlier menarche in PH lesion animals (18.8 ± 0.2 mo) than in sham/controls (25.5 ± 0.9 mo, P < 0.001). Moreover, PH lesion animals had elevated LHRH levels and higher evening glutamate levels after lesions, whereas LHRH changes did not occur in sham/controls until later. Changes in GABA release were not discernible, since evening GABA levels already deceased at 18–20 mo of age in both groups and morning levels remained at the prepubertal levels. The age of first ovulation in both groups did not differ. Collectively, PH lesions may not be a good tool to investigate the mechanism of puberty, and, taking into account the recent findings on the role of kisspeptins, the mechanism of the puberty onset in primates is more complex than we initially anticipated.

scholarly journals Neurobiological Mechanisms of the Onset of Puberty in Primates*

2001 ◽  
Vol 22 (1) ◽  
pp. 111-151 ◽  
Author(s):  
Ei Terasawa ◽  
David L. Fernandez
Keyword(s):  
Rhesus Monkeys ◽  
Neonatal Period ◽  
Developmental Changes ◽  
Neurosecretory System ◽  
Neuronal System ◽  
Inhibitory Neurotransmitter ◽  
Gaba Inhibition ◽  
Female Rhesus ◽  
Lhrh Release ◽  
Low Levels

Abstract An increase in pulsatile release of LHRH is essential for the onset of puberty. However, the mechanism controlling the pubertal increase in LHRH release is still unclear. In primates the LHRH neurosecretory system is already active during the neonatal period but subsequently enters a dormant state in the juvenile/prepubertal period. Neither gonadal steroid hormones nor the absence of facilitatory neuronal inputs to LHRH neurons is responsible for the low levels of LHRH release before the onset of puberty in primates. Recent studies suggest that during the prepubertal period an inhibitory neuronal system suppresses LHRH release and that during the subsequent maturation of the hypothalamus this prepubertal inhibition is removed, allowing the adult pattern of pulsatile LHRH release. In fact,γ -aminobutyric acid (GABA) appears to be an inhibitory neurotransmitter responsible for restricting LHRH release before the onset of puberty in female rhesus monkeys. In addition, it appears that the reduction in tonic GABA inhibition allows an increase in the release of glutamate as well as other neurotransmitters, which contributes to the increase in pubertal LHRH release. In this review, developmental changes in several neurotransmitter systems controlling pulsatile LHRH release are extensively reviewed.

Alveoli increase in number but not size from birth to adulthood in rhesus monkeys

2007 ◽  
Vol 293 (3) ◽  
pp. L570-L579 ◽  
Author(s):  
Dallas M. Hyde ◽  
Shelley A. Blozis ◽  
Mark V. Avdalovic ◽  
Lei F. Putney ◽  
Rachel Dettorre ◽  
...  
Keyword(s):  
Lung Volume ◽  
Rhesus Monkeys ◽  
Developmental Stages ◽  
Lung Parenchyma ◽  
Rate Of Change ◽  
Alveolar Volume ◽  
Lung Volumes ◽  
Male And Female ◽  
Female Rhesus ◽  
Alveolar Duct

Postnatal developmental stages of lung parenchyma in rhesus monkeys is about one-third that of humans. Alveoli in humans are reported to be formed up to 8 yr of age. We used design-based stereological methods to estimate the number of alveoli ( Nalv) in male and female rhesus monkeys over the first 7 yr of life. Twenty-six rhesus monkeys (13 males ranging in age from 4 to 1,920 days and lung volumes from 41.7 to 602 cm3, 13 females ranging in age from 22 to 2,675 days and lung volumes from 43.5 to 380 cm3) were necropsied and lungs fixed, isotropically oriented, fractionated, sampled, embedded, and sectioned for alveolar counting. Parenchymal, alveolar, alveolar duct core air, and interalveolar septal tissue volumes increased rapidly during the first 2 yr with slowed growth from 2 to 7 yr. The rate of change was greater in males than females. Nalv also showed consistent growth throughout the study, with increases in Nalv best predicted by increases in lung volume. However, mean alveolar volume showed little relationship with age, lung volume, or body weight but was larger in females and showed a greater size distribution than in males. Alveoli increase in number but not volume throughout postnatal development in rhesus monkeys.

scholarly journals An Increase in Kisspeptin-54 Release Occurs with the Pubertal Increase in Luteinizing Hormone-Releasing Hormone-1 Release in the Stalk-Median Eminence of Female Rhesus Monkeys in Vivo

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 4151-4157 ◽  
Author(s):  
Kim L. Keen ◽  
Frederick H. Wegner ◽  
Stephen R. Bloom ◽  
Mohammad A. Ghatei ◽  
Ei Terasawa
Keyword(s):  
Median Eminence ◽  
Rhesus Monkeys ◽  
Dependent Manner ◽  
Microdialysis Probe ◽  
Female Rhesus ◽  
Nocturnal Increase ◽  
Pooled Samples ◽  
G Protein Coupled ◽  
Dose Dependent

The G-protein coupled receptor GPR54 and its ligand, KiSS-1-derived peptide kisspeptin-54, appear to play an important role in the mechanism of puberty. This study measures the release of kisspeptin-54 in the stalk-median eminence (S-ME) during puberty and examines its potential role in the pubertal increase in LHRH-1 release in female rhesus monkeys. First, developmental changes in release of kisspeptin-54 and LHRH-1 were assessed in push-pull perfusate samples obtained from the S-ME of prepubertal, early pubertal, and midpubertal female rhesus monkeys. Whereas LHRH-1 levels in 10-min intervals had been measured previously for other experiments, kisspeptin-54 levels in 40-min pooled samples were newly measured by RIA. The results indicate that a significant increase in kisspeptin-54 release occurred in association with the pubertal increase in LHRH-1 release and that a nocturnal increase in kisspeptin-54 release was already observed in prepubertal monkeys and continued through the pubertal period. Second, we measured kisspeptin-54 release in the S-ME of midpubertal monkeys at 10-min intervals using a microdialysis method. Kisspeptin-54 release in the S-ME was clearly pulsatile with an interpulse interval of about 60 min, and approximately 75% of kisspeptin-54 pulses were correlated with LHRH-1 pulses. Finally, the effect of kisspeptin-10 on LHRH-1 release was examined with the microdialysis method. Kisspeptin-10 infusion through a microdialysis probe significantly stimulated LHRH-1 release in a dose-dependent manner. Collectively, the results are consistent with the hypothesis that kisspeptin plays a role in puberty.

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