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  • Author: F. E. Wilson x
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F. E. Wilson

ABSTRACT

A series of experiments was performed to clarify whether photorefractoriness in male tree sparrows is maintained by an androgen-dependent mechanism. Castration did not raise plasma LH in photorefractory males held under a daily photoperiod of 20 h light: 4 h darkness (20L: 4D). Castrated photorefractory males were implanted with the antiandrogen cyproterone or injected s.c. with the antiandrogen flutamide to determine whether androgens which may be resistant to castration inhibit LH secretion. Neither cyproterone nor flutamide raised plasma LH above values found in castrated control birds. Castrated photorefractory males were treated with testosterone to determine whether plasma LH in photorefractory males is androgen-suppressible. Concentrations of plasma LH were independent of plasma testosterone over a wide range of concentrations. The lack of LH response to castration, to castration coupled with antiandrogen therapy, and to castration coupled with testosterone replacement argues that photorefractoriness in male tree sparrows is maintained by an androgen-independent mechanism.

J. Endocr. (1985) 107, 137–143

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F. E. Wilson

ABSTRACT

Photoperiodic control of gonadotrophin secretion in male tree sparrows was studied by examining changes in plasma LH in castrated birds retained on short daylengths and in castrated birds transferred to long daylengths. Plasma LH concentrations were markedly higher in photostimulated birds than in non-photostimulated birds throughout the 25-day experiment, and implantation of the antiandrogen cyproterone (free alcohol), which should have blocked the action of castration-resistant androgens, did not increase plasma LH in either group. Such results, obtained from birds in which testosterone feedback was inoperative, indicate that the gonadostimulatory effect of long daylengths in intact males must be mediated, at least in part, by an androgen feedback-independent mechanism. To determine whether changes in testosterone feedback facilitate gonadotrophin secretion during photostimulation, two feedback performance characteristics (i.e. set point (minimum concentration of testosterone that suppresses plasma LH) and sensitivity (change in plasma LH per unit change in testosterone)) were quantified by evaluating plasma LH responses of non-photostimulated castrated birds and of photostimulated castrated birds to replacement testosterone (0–4·16 μmol). The data indicate that, in addition to stimulating LH secretion by an androgen feedback-independent mechanism, long daylengths reduce feedback inhibition of LH secretion by increasing the putative set point and decreasing the sensitivity of the testosterone feedback mechanism. The feedback-independent effect is the predominant effect of photostimulation on LH secretion in male tree sparrows.

J. Endocr. (1985) 105, 141–152

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F. E. Wilson

ABSTRACT

Testosterone sensitivity of the seminal sacs of castrated tree sparrows from each of three reproductive states was evaluated by measuring the change in seminal-sac mass per unit change in the logarithm of replacement or plasma testosterone. Birds were exposed to exogenous testosterone for 38 days. Replacement doses less than 0·17 μmol or plasma concentrations less than about 0·7 nmol/l did not induce seminal-sac growth in photosensitive castrated birds held on short days, in photosensitive castrated birds transferred from short to long days, or in photorefractory castrated birds retained on long days. Higher replacement doses or plasma concentrations, however, stimulated log dose-dependent growth of the seminal sacs in castrated birds from all three reproductive states. The change in seminal-sac mass per unit change in the logarithm of the dose of replacement testosterone was less (P= 0·0495) in photosensitive castrated birds held on short days than in photosensitive castrated birds transferred to long days. A more critical test of sensitivity (i.e. the change in seminal-sac mass per unit change in the logarithm of mean plasma testosterone concentration) indicated, however, that sensitivity of the seminal sacs to testosterone is independent of reproductive state. That result, when considered in the context of the plasma testosterone profile of intact males during a simulated reproductive cycle, argues that the seminal sacs of sexually quiescent (photosensitive or photorefractory) tree sparrows are small not because of their insensitivity to androgens, but because of a deficiency of circulating androgens.

J. Endocr. (1986) 109, 125–131

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F. E. Wilson

ABSTRACT

An experiment was performed to determine whether photorefractoriness in male tree sparrows is triggered by a testosterone-independent reduction in net photoperiodic drive or by a photoperiod-induced hypersensitivity of the hypothalamic-pituitary axis to testosterone negative feedback. Photosensitive male tree sparrows were transferred from 8 h light: 16 h darkness (8L: 16D) to 20L: 4D. Birds were castrated bilaterally on day 28 of photostimulation. Beginning on day 33 and weekly thereafter until day 54, birds were given replacement testosterone (0–1·49 μmol) in s.c. polydimethylsiloxane capsules. Plasma samples collected on days 36, 43, 50 and 57 were assayed for LH. Plasma LH concentrations in birds without replacement testosterone were regarded as reflecting net photoperiodic drive in the absence of testosterone feedback, and the slopes of curves relating the logarithm of plasma LH concentration to dose of replacement testosterone were taken as quantitative measures of testosterone feedback sensitivity. The results showed that a testosterone-independent reduction in net photoperiodic drive beginning between days 43 and 50 preceded any change in sensitivity to testosterone negative feedback. Such results provide compelling evidence that a testosterone-independent mechanism triggers the photorefractory state in male tree sparrows.

J. Endocr. (1986) 109, 133–137

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E. C. Osborn, P. L. Sugden, J. C. Mackenzie, D. M. Aitken, I. D. Chapman, S. Howes, O. F. Mason, G. V. Rigby and J. Wilson

ABSTRACT

Angiotensin II and I significantly raised potassium and lowered sodium and chloride ion concentrations in arterial plasma, with peak changes occurring in the first 2 min of a 6-min infusion period. The octapeptide increased the arterial K+ level in a dose-dependent manner, but the response showed tachyphylaxis when multiple infusions of 6-min duration were administered after a recovery interval of only 5 min. Raising the arterial blood pressure by 20–33 mmHg with adrenaline and noradrenaline failed to account for the increase in arterial plasma K+ concentration produced by the two peptides. These findings, in particular the rise in K+ concentration, are discussed in relation to possible mechanisms by which angiotensin II affects arteriolar tone.

J. Endocr. (1985) 104, 143–148

Free access

D S Gardner, B W M Van Bon, J Dandrea, P J Goddard, S F May, V Wilson, T Stephenson and M E Symonds

Glucocorticoids are proposed to act as intermediary factors that transcribe the developmental programming sequelae of maternal nutrient restriction (NR). Periconceptional under-nutrition of sheep markedly activates fetal hypothalamic–pituitary–adrenal (HPA) axis activity leading to preterm birth, while transient undernutrition during late gestation in sheep programs adult HPA axis function. To date, no study has examined resting or stimulated HPA axis function in young adult offspring following a periconceptional nutritional challenge. In the present study, 20 ewes were either periconceptionally undernourished (50% metabolisable energy requirements from days 1 to 30 gestation; NR, n = 8) or fed to control levels (100% requirement; controls, n = 12) to term (147 days gestation). Ewes were blood sampled remotely at 2 and 30 days using automated blood sampling equipment. Thereafter, offspring (controls, n = 6/6 males/females; NR, n = 4/4 males/females) were reared to 1 year of age and on separate days received either an i.v. corticotrophin-releasing hormone (CRH; 0.5 μg/kg) and vasopressin (AVP; 0.1 μg/kg) challenge or a synthetic ACTH i.v. bolus (Synacthen; 1.25 μg/kg), and blood samples were taken (manually and remotely) at appropriate intervals for measurement of plasma ACTH and cortisol accordingly. Resting plasma cortisol, assessed remotely, was similar in ewes during undernutrition (control 18.3 ± 1.4 vs NR 23.4 ± 1.9 nmol/l) and in offspring at 4 months of age (control male 17.6 ± 2.9; control female 17.2 ± 0.4, NR male 16.5 ± 3.1, NR female 21.7 ± 4.0 nmol/l). At 12 months of age, however, resting plasma cortisol was significantly increased in NR females (control male 28.0 ± 1.5, control female 32.9 ± 9, NR male 32 ± 7, NR female 53 ± 10 nmol/l, F 5.7, P = 0.02) despite no difference in plasma ACTH concentration. There was an interaction between nutritional group and gender for both the pituitary and adrenal responses to CRH and AVP, i.e. for controls, females exhibited increased plasma ACTH or cortisol relative to males but for NR this trend was either not present or reversed. The adrenocortical response to synthetic ACTH was gender-dependent only, being greater in female offspring. Combined CRH and AVP provoked a transient hypertension and marked bradycardia in all animals, irrespective of dietary group or gender and could be effectively reproduced by an AVP bolus alone. In conclusion, the present study has shown that periconceptional undernutrition of sheep has only a minor influence on HPA axis function in their young adult offspring when considered alongside the effect of gender per se.

Open access

K S Wilson, C S Tucker, E A S Al-Dujaili, M C Holmes, P W F Hadoke, C J Kenyon and M A Denvir

Glucocorticoids (GCs) in utero influence embryonic development with consequent programmed effects on adult physiology and pathophysiology and altered susceptibility to cardiovascular disease. However, in viviparous species, studies of these processes are compromised by secondary maternal influences. The zebrafish, being fertilised externally, avoids this problem and has been used here to investigate the effects of transient alterations in GC activity during early development. Embryonic fish were treated either with dexamethasone (a synthetic GC), an antisense GC receptor (GR) morpholino (GR Mo), or hypoxia for the first 120h post fertilisation (hpf); responses were measured during embryonic treatment or later, post treatment, in adults. All treatments reduced cortisol levels in embryonic fish to similar levels. However, morpholino- and hypoxia-treated embryos showed delayed physical development (slower hatching and straightening of head–trunk angle, shorter body length), less locomotor activity, reduced tactile responses and anxiogenic activity. In contrast, dexamethasone-treated embryos showed advanced development and thigmotaxis but no change in locomotor activity or tactile responses. Gene expression changes were consistent with increased (dexamethasone) and decreased (hypoxia, GR Mo) GC activity. In adults, stressed cortisol values were increased with dexamethasone and decreased by GR Mo and hypoxia pre-treatments. Other responses were similarly differentially affected. In three separate tests of behaviour, dexamethasone-programmed fish appeared ‘bolder’ than matched controls, whereas Mo and hypoxia pre-treated fish were unaffected or more reserved. Similarly, the dexamethasone group but not the Mo or hypoxia groups were heavier, longer and had a greater girth than controls. Hyperglycaemia and expression of GC responsive gene (pepck) were also increased in the dexamethasone group. We conclude that GC activity controls many aspects of early-life growth and development in the zebrafish and that, like other species, manipulating GC status pharmacologically, physiologically or genetically in early life leads to programmable metabolic and behavioural traits in adulthood.