collected from the tail tip, every 10 min over 4 h, starting 2 h before lights off. To assess LH surge amplitude in females, four blood samples (four microliters each) were collected from the tail tip over 10 consecutive days: at 10:00 h and at 18:00, 19
Chirine Toufaily, Gauthier Schang, Xiang Zhou, Philipp Wartenberg, Ulrich Boehm, John P Lydon, Ferdinand Roelfsema and Daniel J Bernard
K Rousseau, Z Atcha, J Denton, F R A Cagampang, A R Ennos, A J Freemont and A S I Loudon
.1 Newtons SD leptin versus 52 ± 4.5 Newtons SD PBS). Discussion Our data show that despite remarkable natural high amplitude changes in adiposity and circulating leptin concentrations, this was not associated with any
Jonathan D Johnston and Debra J Skene
, this leads to high amplitude rhythms in pineal Aa-nat mRNA abundance ( Borjigin et al . 1995 , Coon et al . 1995 ) indicating that AA-NAT synthesis is a major mechanism driving the melatonin synthesis rhythm. However melatonin synthesis in all
C. Meyer, M. J. Freund-Mercier, Y. Guerné and Ph. Richard
Plasma concentrations of oxytocin and vasopressin were measured in relationship to oxytocin cell firing during suckling in urethane-anaesthetized rats.
Preliminary experiments showed that plasma concentrations of oxytocin and vasopressin, which were increased immediately after anaesthesia, reverted to basal concentrations 3 h later. Moreover, it was found that exogenous oxytocin had entirely disappeared 5 min after i.v. bolus injections of known doses of oxytocin.
Suckling did not modify the basal plasma concentration of oxytocin (14·6 ± 2·9 compared with 14·±61·5 pmol/l before suckling) except during a brief period immediately after neurosecretory bursts on oxytocin cells (37·8 ± 5·2 pmol/l; P < 0·001, n = 11). The plasma concentration of oxytocin did not differ significantly from the basal concentration 1·5 min later. The plasma concentration of vasopressin never varied.
After two neurosecretory bursts of similar amplitude (total number of spikes during the burst) recorded on the same oxytocin cell, the variations in plasma concentration of oxytocin were also similar. When, for a given cell, the amplitude of neurosecretory bursts increased or decreased, the amount of oxytocin released changed in the same way.
These data demonstrate (1) that suckling induces pulsatile release of oxytocin without vasopressin, and (2) a direct relationship between the amounts of oxytocin released and the amplitude of oxytocin cell neurosecretory bursts which argue in favour of simultaneous increases or decreases in the neurosecretory burst amplitudes on all oxytocin cells.
J. Endocr. (1987) 114, 263–270
BK Campbell, H Dobson and RJ Scaramuzzi
This study examined the effect of LH pulses, of similar amplitude and frequency to those found in the luteal phase, on the pattern of hormone secretion and follicle development in GnRH antagonist-suppressed ewes stimulated with exogenous FSH. This experiment was conducted on ewes with ovarian autotransplants in a continuous study. Follicle development was suppressed in 18 ewes by 3 weeks of GnRH antagonist treatment (50 micrograms/kg per 4 days s.c.), and was then stimulated by infusion of ovine (o)FSH (5 micrograms NIADDK-oFSH-16/h i.v.) for 3 days. In addition to FSH, 10 animals received pulses of LH (2.5 micrograms NIADDK-oLH-26 i.v.) every 4 h for the entire period of the FSH infusion. The follicle population was determined by daily ultrasound. Samples of ovarian and jugular venous blood were collected at 4-h intervals over the period of the FSH infusion and there were three periods of intensive blood sampling (15-min intervals for 2.5 h at 24, 48 and 72 h after the start of the FSH infusion) when the steroidogenic capacity of the follicles in all 18 ewes was tested around an LH challenge (2.5 micrograms i.v.). GnRH antagonist treatment resulted in a 57% decrease in FSH concentrations and prevented ovarian follicle development beyond 3 mm in diameter. Infusion of FSH resulted in a 60% increase in FSH concentrations and stimulated the development of large antral follicles and a coincident increase in ovarian androstenedione, inhibin and oestradiol secretion in both experimental groups. In the absence of 4-hourly LH pulses basal steroid secretion was negligible (< 1 ng/min; P < 0.001). Daily LH challenges, however, revealed no difference in the steroidogenic capacity of the follicle population in either experimental group. Similarly, LH pulses had no effect on the growth rate and number of antral follicles stimulated by FSH infusion, or the pattern of ovarian inhibin secretion. In conclusion, these results show that while FSH alone can stimulate the development of ovulatory sized follicles in ewes made hypogonadal with GnRH antagonist, physiological patterns of LH stimulation have no deleterious effects on FSH-stimulated follicle development and are essential for normal steroidogenesis.
R. P. McIntosh and J. E. A. McIntosh
Pulse amplitude and frequency are often used to describe measurements of LH in blood. Such analyses are compatible with models of LH being released from the pituitary in episodes that are controlled by pulses of hypothalamic gonadotrophin-releasing hormone. The amplitudes of these secretory episodes as seen in blood are usually defined as the net heights of peaks above a baseline. As a measure of each pituitary secretory episode, this is valid only if peaks are regularly and widely spaced, making overlap negligible. When episodes are erratic and frequent so that only fractions of peaks have been cleared from the circulation before others follow, nadirs between peaks include output from previous episodes and do not define a physiologically meaningful baseline. Applied to overlapping peaks, such measures of amplitude usually underestimate pituitary secretory episodes and imply a tonic mode of LH secretion in addition to pulsatile release.
Using the additional information of fitted LH clearance coefficients to define the shapes of LH peaks, a simple method based on an episodic mode of release alone is described, for estimating more accurately the relative sizes of secretory episodes as observed in blood, free of the effects of overlapping peaks. Using this analysis we have described the variation in amplitude, interval and clearance rates of LH secretory episodes within and between four normal menstrual cycles of a single individual. Thirteen, 3–6 h blood sampling sessions were performed during early follicular growth at the transition from luteal to follicular phases when the frequencies of LH peaks, LH/FSH ratios and progesterone concentrations were changing markedly.
Our secretory episode model described all data well without the need to introduce a tonic mode of release. When frequent pulses overlapped we found that amplitudes of episodes were usually higher than peaks estimated by conventional methods, but a decrease in both amplitude and pulse interval occurred after the start of menstruation. Highly variable patterns of LH release were demonstrated in the late luteal phase of this normal individual while FSH levels rose consistently.
J. Endocr. (1985) 107, 231–239
M. E. Wilson, S. Lackey, K. Chikazawa and T. P. Gordon
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
Obaro Evuarherhe, James Leggett, Eleanor Waite, Yvonne Kershaw and Stafford Lightman
undergo a maturational process during puberty. Whether or not the pubertal maturation of the HPA axis is dependent on the rise in gonadal steroids following the rise in frequency and amplitude of GnRH release or is more related to other maturational
Dan-Dan Feng, Yu-Feng Zhao, Zi-Qiang Luo, Damien J Keating and Chen Chen
increments. VDCC currents were activated at depolarizing potential of −30 mV and reached the maximal level at depolarizing potential of 10 mV. The maximal amplitude and shape of these Ca 2 + currents was not significantly different when cells were stepped
Se Hee Min, Jung Hee Kim, Yu Mi Kang, Seung Hak Lee, Byung-Mo Oh, Kyou-Sup Han, Meihua Zhang, Hoe Suk Kim, Woo Kyung Moon, Hakmo Lee, Kyong Soo Park and Hye Seung Jung
and the tibial nerve at the posterior ankle area. Onset latencies and base-to-peak amplitudes of compound muscle action potentials (CMAP) of the gastrocnemius muscle were measured using recording electrodes (Digital Ring Electrode, Scalp Needle