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.

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 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.

The amplitude of nocturnal melatonin concentrations is not decreased by oestradiol and does not alter reproductive function in adolescent or adult female rhesus monkeys

1993 ◽  
Vol 137 (2) ◽  
pp. 299-309 ◽  
Author(s):  
M. E. Wilson ◽  
S. Lackey ◽  
K. Chikazawa ◽  
T. P. Gordon
Keyword(s):  
Replacement Therapy ◽  
Rhesus Monkeys ◽  
Pubertal Development ◽  
Developmental Changes ◽  
Ovulatory Cycle ◽  
Serum Samples ◽  
Night Time ◽  
Serum Progesterone ◽  
Female Rhesus ◽  
Igf I

ABSTRACT Nocturnal concentrations of melatonin in serum decline significantly with advancing pubertal development in both children and non-human primates and elevated levels may be associated with anovulation in adults. Three studies, using female rhesus monkeys, were performed to determine whether (1) the decline in nocturnal melatonin concentrations in adolescents was due to maturational increases in serum oestradiol, (2) the experimental elevation in nocturnal melatonin would delay the normal progression of puberty in post-menarchial monkeys, and (3) the experimental elevation in nocturnal melatonin would disrupt normal ovulatory function in adults. In experiment 1, juvenile female rhesus monkeys, housed indoors in a fixed photoperiod (12 h light: 12 h darkness), were assigned randomly to one of two treatment groups: ovariectomized with no replacement therapy (control; n= 4) or ovariectomized with oestradiol replacement therapy maintaining oestradiol at ∼ 90 pmol/l (treated; n= 8). Twenty-four hour as well as daytime serum samples were collected from 19 to 35 months of age. Nocturnal melatonin concentrations declined significantly in all females with advancing chronological age and this change was unaffected by oestradiol treatment. The decline in nocturnal melatonin concentrations occurred, on average, 2·0 ±0·2 months after the initial rise in serum LH in control females and 6·0 ±0·8 months in treated females. Furthermore, this decline in night-time melatonin was not related to significant developmental changes in body weight. In experiment 2, control (n = 6) and melatonintreated (treated; n =6) adolescent female monkeys were studied from −30 to +105 days from menarche. Beginning at 45 days following menarche, treated females received 30 days of nocturnal melatonin infusion to elevate levels to prepubertal values. Developmental changes in perineal swelling and coloration as well as serum oestradiol and insulin-like growth factor-I (IGF-I) were compared with values observed during the 45-day pretreatment and 30-day post-treatment conditions as well as with those observed in control females. Despite a significant elevation in nightly melatonin levels for the 30-day period in treated females, developmental changes in oestradiol, IGF-I, and perineal coloration and swelling were not different compared with the control females. In experiment 3, adult females were given melatonin nightly beginning on the first day of menses following an ovulatory cycle and treatment was continued for 45 days or until the next menstruation occurred. Melatonin was elevated to supraphysiological levels every night throughout the treatment period. Despite this elevation, an ovulation, inferred from serum progesterone levels, occurred in every female and serum oestradiol, LH or progesterone were not affected compared with the values obtained during the untreated cycle. These data indicate that the decline in nocturnal melatonin concentrations is not related to a developmental increase in oestradiol secretion. Furthermore, experimentally elevated concentrations of nocturnal melatonin did not delay the normal progression of puberty following menarche nor did it disrupt ovulatory function in adults. These data suggest that the enhanced nocturnal melatonin concentrations are not causally linked to either puberty onset or anovulatory conditions in adults. Journal of Endocrinology (1993) 137, 299–309

Androgen Receptors in the Cerebral Cortex of Fetal Female Rhesus Monkeys*

Endocrinology ◽  
1986 ◽  
Vol 119 (4) ◽  
pp. 1625-1631 ◽  
Author(s):  
SAMUEL A. SHOLL ◽  
STEVEN M. POMERANTZ
Keyword(s):  
Cerebral Cortex ◽  
Rhesus Monkeys ◽  
Androgen Receptors ◽  
Female Rhesus

THE EFFECTS OF DEXAMETHASONE AND ANDROGENS ON SEXUAL RECEPTIVITY OF FEMALE RHESUS MONKEYS

1971 ◽  
Vol 51 (3) ◽  
pp. 575-588 ◽  
Author(s):  
B. J. EVERITT ◽  
J. HERBERT
Keyword(s):  
Rhesus Monkeys ◽  
Testosterone Propionate ◽  
Secretory Activity ◽  
Urinary Free Cortisol ◽  
Sexual Receptivity ◽  
Adrenal Androgens ◽  
Electrolyte Metabolism ◽  
Free Cortisol ◽  
Female Rhesus ◽  
The Central Nervous System

SUMMARY The effect of dexamethasone, given either alone or together with testosterone propionate or androstenedione, was studied in nine female rhesus monkeys (paired with three males) by making quantitative observations on behaviour in the laboratory. Dexamethasone (0·5 mg/kg/day) given to oestrogen-treated ovariectomized female monkeys made them sexually unreceptive, and there was an associated decline in the level of the male's mounting activity. Testosterone propionate (100 or 200 μg/day) reversed completely the effects of dexamethasone on sexual behaviour. Androstenedione (100, 200 or 400 μg/day) had similar, but less marked, effects whereas cortisol (10 mg/day) or progesterone (100, 200 or 500 μg/day) were ineffective. Treating a female with testosterone prevented dexamethasone from reducing sexual receptivity. Parallel determinations of urinary free cortisol showed that the dexamethasone had suppressed the secretory activity of the adrenal cortex. There were no consistent changes, under any treatment, in the females' vaginal epithelia, sexual skins or clitorides, or in their water or electrolyte metabolism. These findings indicate that adrenal androgens regulate sexual receptivity in these female primates, probably by an action on the central nervous system.

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