Developmental Changes in the Luteinizing Hormone Secretory Pattern in Peripubertal Female Rhesus Monkeys: Comparisons between Gonadally Intact and Ovariectomized Animals*

Abstract. Suppression of luteinizing hormone (LH) by sc implanted oestradiol-17ß (E2) pellets was examined in 4 ovariectomized female rhesus monkeys during the breeding season, the non-breeding season and during the transition between the breeding and non-breeding season. Immunoreactive LH was suppressed to 58, 78 and 75% of untreated levels for the respective seasonal conditions. Bioactive LH was suppressed to 29, 49 and 33% of baseline. Bioactive LH (determined by testoster-one release from rat interstital cells) was significantly correlated (r = 0.84) with immunoactive LH from the same samples. It is concluded that E2 treatment of ovariectomized female rhesus monkeys results in suppressed levels of LH, regardless of the time of year.

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Neurobiological Mechanisms of the Onset of Puberty in Primates*

Endocrine Reviews ◽

10.1210/edrv.22.1.0418 ◽

2001 ◽

Vol 22 (1) ◽

pp. 111-151 ◽

Cited By ~ 4

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.

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Role of glutamic acid decarboxylase in the prepubertal inhibition of the luteinizing hormone releasing hormone release in female rhesus monkeys

Journal of Neuroscience ◽

10.1523/jneurosci.16-08-02563.1996 ◽

1996 ◽

Vol 16 (8) ◽

pp. 2563-2573 ◽

Cited By ~ 50

Author(s):

D Mitsushima ◽

F Marzban ◽

LL Luchansky ◽

AJ Burich ◽

KL Keen ◽

...

Keyword(s):

Luteinizing Hormone ◽

Glutamic Acid ◽

Glutamic Acid Decarboxylase ◽

Rhesus Monkeys ◽

Acid Decarboxylase ◽

Hormone Release ◽

Luteinizing Hormone Releasing Hormone ◽

Releasing Hormone ◽

Female Rhesus

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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 ◽

10.1210/en.2011-1565 ◽

2012 ◽

Vol 153 (2) ◽

pp. 825-836 ◽

Cited By ~ 67

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.

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