Central action of thyrotrophin-releasing hormone on growth hormone secretion in domestic fowl

1990 ◽  
Vol 126 (1) ◽  
pp. 83-88 ◽  
Author(s):  
S. Harvey ◽  
R. W. Lea ◽  
C. Ahene

ABSTRACT Peripheral plasma concentrations of GH in adult chickens were increased, in a dose-related manner, between 5 and 30 min after the intracerebroventricular (i.c.v.) injection of 0·1 or 10 μg TRH. In contrast, i.v. administration of comparable doses of TRH had no significant effect on circulating GH concentrations. [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) was located in the pituitary gland and peripheral plasma within 5 min of its i.c.v. administration, although in amounts that were unlikely to affect directly pituitary function. [3H]Me-TRH rapidly accumulated in the hypothalamus following its i.c.v. administration (but not after i.v. injection), and the central effect of TRH on GH secretion in birds is therefore likely to be induced by effects at hypothalamic sites. Journal of Endocrinology (1990) 126, 83–88

1981 ◽  
Vol 97 (4) ◽  
pp. 448-453 ◽  
Author(s):  
C. G. Scanes ◽  
S. Harvey ◽  
B. A. Morgan ◽  
M. Hayes

Abstract. Variations in plasma growth hormone (GH) concentrations following iv or sc administration of synthetic thyrotrophin-releasing hormone (TRH, Pyr-His-Pro-NH2) have been followed in immature and adult domestic fowl. TRH markedly stimulated GH secretion in newly hatched (1 and 2 day old) chicks and in 6-week-old cockerels but in adult male or female birds of two strains had very little effect, if any. Intravenous injection of 4 TRH analogues (Pyr-His-Mep-NH2, Pyr-Meh-Mep-NH2, Pyr-Meh-Mep-NH and Pyr-Meh-Pro-NH2) were also potent GH secretagogues in 6-week-old birds. The stimulatory effect of TRH or the TRH-analogues on GH secretion was not dose-related.


1981 ◽  
Vol 89 (3) ◽  
pp. 405-410 ◽  
Author(s):  
S. HARVEY ◽  
R. J. STERLING ◽  
J. G. PHILLIPS

Age-related changes in the response of GH to administration of thyrotrophin releasing hormone (TRH) have been investigated in the domestic fowl. In two strains of chicken the i.v. administration of TRH (10 μg/kg) to 4-week-old male and female birds markedly increased (> 200 ng/ml) the plasma GH concentration within 10 min of treatment and the concentration remained higher than the pretreatment level for at least a further 20 min. Saline (0·9%) administration had no effect on GH secretion in comparable groups of control birds. The same dose of TRH had no effect on plasma GH concentrations in adult (> 24-week-old) laying hens or cockerels. The administration of TRH at doses of 0·1–100 μg/kg (i.v.) or 0·39–50 μg/bird (s.c.) also had very little, if any, effect on GH secretion in laying hens. In laying hens slight increases (10–20 ng/ml, P < 0·05) in the plasma concentrations of GH were observed in one experiment 60 min after the s.c. injection of 100 μg TRH, and in another 60, 90 and 120 min after the serial s.c. injection of TRH (100 μg/bird) every 30 min over a 150 min period. The poor GH response of the adults to TRH stimulation was not due to high circulating concentrations of endogenous gonadal steroids, as surgical gonadectomy had no effect on the GH response to TRH. These results suggest maturational differences in the control of GH secretion in the fowl.


1986 ◽  
Vol 111 (1) ◽  
pp. 91-97 ◽  
Author(s):  
S. Harvey ◽  
S.-K. Lam ◽  
T. R. Hall

ABSTRACT Passive immunization of immature chickens with sheep somatostatin (SRIF) antiserum promptly increased the basal plasma GH concentration and augmented TRH-induced GH secretion. Although exogenous SRIF had no inhibitory effect on the basal GH concentration in untreated birds or birds pretreated with non-immune sheep serum, it suppressed the stimulatory effect of SRIF immunoneutralization on GH secretion. These results suggest that SRIF is physiologically involved in the control of GH secretion in birds, in which it appears to inhibit GH release tonically. J. Endocr. (1986) 111, 91–97


1985 ◽  
Vol 105 (3) ◽  
pp. 351-355 ◽  
Author(s):  
H. Klandorf ◽  
S. Harvey ◽  
H. M. Fraser

ABSTRACT Immature cockerels (4- to 5-weeks old) were passively immunized, with antiserum raised in sheep, against thyrotrophin-releasing hormone (TRH). The administration of TRH antiserum (anti-TRH) at doses of 0·5, 1·0 or 2·0 ml/kg lowered, within 1 h, the basal concentration of plasma GH for at least 24 h. The administration of normal sheep serum had no significant effect on the GH concentration in control birds. Although the GH response to TRH (1·0 or 10·0 μg/kg) was not impaired in birds treated 1 h previously with anti-TRH, prior incubation (at 39 °C for 1 h) of TRH (20 μg/ml) with an equal volume of anti-TRH completely suppressed the stimulatory effect of TRH (10 pg/kg) on GH secretion in vivo. These results suggest that TRH is physiologically involved in the hypothalamic control of GH secretion in the domestic fowl. J. Endocr. (1985) 105, 351–355


1993 ◽  
Vol 138 (1) ◽  
pp. 137-147 ◽  
Author(s):  
S. Harvey ◽  
V. L. Trudeau ◽  
R. J. Ashworth ◽  
S. M. Cockle

ABSTRACT Pyroglutamylglutamylprolineamide (pGlu-Glu-ProNH2) is a tripeptide with structural and immunological similarities to thyrotrophin-releasing hormone (TRH; pGlu-His-ProNH2). Since TRH stimulates GH secretion in domestic fowl, the possibility that pGlu-Glu-ProNH2 may also provoke GH release was investigated. Unlike TRH, pGlu-Glu-ProNH2 alone had no effect on GH release from incubated chicken pituitary glands and did not down-regulate pituitary TRH receptors. However, pGlu-Glu-ProNH2 suppressed TRH-induced GH release from pituitary glands incubated in vitro and competitively displaced [3H]methyl3-histidine2-TRH from pituitary membranes. Systemic injections of pGlu-Glu-ProNH2 had no significant effect on basal GH concentrations in conscious birds, but promptly lowered circulating GH levels in sodiumpentobarbitone anaesthetized fowl. Submaximal GH responses of conscious and anaesthetized birds to systemic TRH challenge were, however, potentiated by prior or concomitant administration of pGlu-Glu-ProNH2. These results demonstrate, for the first time, that pGlu-Glu-ProNH2 has biological activity, with inhibitory and stimulatory actions within the avian hypothalamo-pituitary axis. These results indicate that pGlu-Glu-ProNH2 may act as a TRH receptor antagonist within this axis. Journal of Endocrinology (1993) 138, 137–147


2000 ◽  
Vol 165 (2) ◽  
pp. 337-344 ◽  
Author(s):  
SS Rizvi ◽  
GF Weinbauer ◽  
M Arslan ◽  
CJ Partsch ◽  
E Nieschlag

We investigated a possible modulation of growth hormone (GH) secretion by testosterone by measuring the growth hormone releasing hormone (GHRH)-stimulated and N-methyl-d,l-aspartic acid (NMA)-induced GH secretion in adult rhesus monkeys. Intact, orchidectomized and testosterone-substituted (testosterone enanthate 125 mg/week, i.m. for 5 weeks) orchidectomized monkeys (n=5) were used in the study. GHRH (25 microg/kg body weight) or NMA (15 mg/kg body weight) was infused through a Teflon cannula implanted in the saphenous vein. Sequential blood samples were collected 30-60 min before and 60 min after the injection of the neurohormone or the drug at 10-20-min intervals. All bleedings were carried out under ketamine hydrochloride anaesthesia (initial dose 5 mg/kg body weight i.m., followed by 2.5 mg/kg at 30-min intervals). The plasma concentrations of GH, testosterone and oestradiol (E(2)) were determined by using specific assay systems. Administration of GHRH elicited a significant increase in GH secretion in all three groups of animals. There was no significant difference in the responsiveness of pituitary somatotrophs to exogenous GHRH challenges between intact and orchidectomized monkeys and testosterone replacement in orchidectomized animals did not significantly alter the GHRH-induced GH response. The responsiveness of hypothalamic GHRH neurones apparently did undergo a qualitative change after orchidectomy, as GH response to NMA was less in orchidectomized animals than in intact monkeys. The responsiveness of GHRH neurones to exogenous NMA was restored and even potentiated when orchidectomized monkeys were treated with testosterone. Taken together, these findings suggest that testosterone does not affect the sensitivity of the pituitary somatotrophs to GHRH but stimulates the secretion of GH by modulation of the NMDA drive to GHRH neurones.


1986 ◽  
Vol 108 (3) ◽  
pp. 413-416 ◽  
Author(s):  
C. G. Scanes ◽  
S. Harvey ◽  
J. Rivier ◽  
W. Vale

ABSTRACT Rat hypothalamic GH-releasing factor (rhGRF), at doses between 0·1 and 10 μg/kg, increased plasma GH concentrations in immature domestic fowl 5–10 min after i.v. injection. Sodium pentobarbitone anaesthesia blunted the GH responses to rhGRF, although in both conscious and anaesthetized chicks the maximal responses were induced by a dose of 1 μg rhGRF/kg. The stimulatory effect of rhGRF on in-vivo GH secretion was less than that provoked by corresponding doses of human pancreatic GRF, but greater than that elicited by two rhGRF analogues, (Nle27)-rhGRF(1–32) and (Nle27)-rhGRF(1–29). These results demonstrate that the chicken pituitary is responsive to mammalian GRF and provide evidence of structure-activity relationships of GRF in the domestic fowl. J. Endocr. (1986) 108, 413–416


1983 ◽  
Vol 96 (2) ◽  
pp. 329-334 ◽  
Author(s):  
S. Harvey

The influence of thyroxine (T4) and tri-iodothyronine (T3) on the secretion of GH in immature fowl was investigated. In birds pretreated with i.m. injections of T4 (100 μg/day for 10 days or 250 μg/kg for 7 days) or T3 (250 μg/kg for 7 days) the basal plasma GH level was markedly reduced. A similar reduction in the basal plasma GH level was also observed 60 min after a single injection or T3 (25 and 250 μg/kg) or T4 (250 μg/kg). In control birds the concentration of plasma GH was greatly increased (> 450 μg/l) within 10 min of an i.v. injection of thyrotrophin releasing hormone (TRH; 10 μg/kg). In birds pretreated with T3 or T4 the increase in GH concentration after TRH treatment was significantly less than that in the controls. In birds pretreated for 60 min with T3 or T4 the GH response to TRH was inversely dose-related and lowest in T3-treated birds. These results demonstrate that T3 and T4 inhibit GH secretion in birds, which is an effect not observed in mammalian species.


1992 ◽  
Vol 135 (2) ◽  
pp. 371-382 ◽  
Author(s):  
R. Vasilatos-Younken ◽  
P. H. Tsao ◽  
D. N. Foster ◽  
D. L. Smiley ◽  
H. Bryant ◽  
...  

ABSTRACT The ability of continuously delivered GH-releasing factor (GRF) to enhance GH secretion while maintaining the normal ultradian GH rhythm was investigated. Synthetic human GH-releasing factor (hGRF(1–44)NH2) was continuously infused for 4 days by means of i.v. catheters to 11-week-old broiler chickens. At this age, overall endogenous GH secretion is low, and baseline GH is barely detectable. Six birds per treatment received vehicle (control), 0·324 mg hGRF(1–44)NH2/kg body weight per day (low dose) or 3·24 mg hGRF(1–44)NH2/kg body weight per day (high dose). After 4 days of GRF conditioning, concurrent with continued GRF infusion, serial blood samples were removed via atrial catheters at 15-min intervals for 6 h and GH plasma profiles determined. High dose GRF significantly increased GH plasma concentrations over tenfold compared with controls; however, most of this increase reflected an increase in basal GH, which was reinstated to juvenile baseline levels. Augmentation of pulse amplitude above this increased baseline was not proportionately as high, and failed to reach juvenile levels. The ultradian rhythm of GH was not altered by continuous GRF administration. Both low and high dose GRF treatments resulted in significant enlargement of the anterior pituitary gland. Total pituitary GH mRNA levels, although elevated over twofold by GRF treatment, were not significantly different from controls. Measures of plasma GH magnitude (overall and baseline mean, and peak amplitude) were significantly correlated with pituitary GH mRNA for control birds, but were not correlated for GRF treatments. Feed intake was markedly depressed (33%) on the high dose GRF treatment, in conjunction with total inhibition of body weight gain over the 4-day period of administration. Longitudinal bone growth and width of the epiphyseal growth plate were also significantly reduced by high dose GRF treatment, probably reflecting the reduced level of nutrient intake, despite high circulating concentrations of GH. Journal of Endocrinology (1992) 135, 371–382


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