pGlutamylglutamylprolineamide modulation of growth hormone secretion in domestic fowl: antagonism of thyrotrophin-releasing hormone action?

1993 ◽  
Vol 138 (1) ◽  
pp. 137-147 ◽  
Author(s):  
S. Harvey ◽  
V. L. Trudeau ◽  
R. J. Ashworth ◽  
S. M. Cockle
Keyword(s):  
Domestic Fowl ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Concomitant Administration ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Pituitary Glands ◽  
First Time

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

Effect of synthetic thyrotrophin-releasing hormone and its analogues on growth hormone secretion in the domestic fowl (Gallus Domesticus)

1981 ◽  
Vol 97 (4) ◽  
pp. 448-453 ◽  
Author(s):  
C. G. Scanes ◽  
S. Harvey ◽  
B. A. Morgan ◽  
M. Hayes
Keyword(s):  
Growth Hormone ◽  
Domestic Fowl ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Gallus Domesticus ◽  
Plasma Growth Hormone ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Trh Analogues

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.

Physiological control of growth hormone secretion by thyrotrophin-releasing hormone in the domestic fowl

1985 ◽  
Vol 105 (3) ◽  
pp. 351-355 ◽  
Author(s):  
H. Klandorf ◽  
S. Harvey ◽  
H. M. Fraser
Keyword(s):  
Domestic Fowl ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Physiological Control ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Normal Sheep Serum ◽  
Plasma Gh

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

DIMINUTION OF THYROTROPHIN RELEASING HORMONE-INDUCED GROWTH HORMONE SECRETION IN ADULT DOMESTIC FOWL (GALLUS DOMESTICUS)

1981 ◽  
Vol 89 (3) ◽  
pp. 405-410 ◽  
Author(s):  
S. HARVEY ◽  
R. J. STERLING ◽  
J. G. PHILLIPS
Keyword(s):  
Domestic Fowl ◽  
Laying Hens ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Growth Hormone Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Age Related ◽  
Plasma Gh

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.

Benzodiazepine antagonism of thyrotrophin-releasing hormone receptors: biphasic actions on growth hormone secretion in domestic fowl

1993 ◽  
Vol 137 (1) ◽  
pp. 35-42 ◽  
Author(s):  
S. Harvey
Keyword(s):  
Binding Sites ◽  
Domestic Fowl ◽  
Benzodiazepine Receptors ◽  
Growth Hormone Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Central Type ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Pituitary Glands

ABSTRACT Benzodiazepines are pharmacological agents widely used for their anxiolytic and anticonvulsant properties. However, as these drugs are known to antagonize the binding and action of thyrotrophin-releasing hormone (TRH) in pituitary tissue, the possibility that they may modulate GH secretion was investigated in domestic fowl, in which TRH is a GH-releasing factor. Chlordiazepoxide (an antagonist of central-type benzodiazepine receptors) had no significant effect on the basal release of GH from incubated chicken pituitary glands, but at concentrations > 10 μmol/l chlordiazepoxide suppressed somatotroph responsiveness and sensitivity to TRH stimulation. At this concentration, chlordiazepoxide competitively displaced the binding of [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) to chicken pituitary membranes. The prior incubation of pituitary glands with chlordiazepoxide had no significant effect on the number of [3H]Me-TRH-binding sites, which were also unaffected by the administration of chlordiazepoxide in vivo. However, contrary to its effects in vitro, chlordiazepoxide reduced basal GH secretion in vivo, whilst potentiating the GH response to systemic TRH challenge. These results demonstrate benzodiazepine antagonism of TRH-binding sites in domestic fowl and a biphasic modulation of GH secretion, which may be mediated through opposing actions at pituitary and central sites. Journal of Endocrinology (1993) 137, 35–42

Thyrotrophin-releasing hormone-induced growth hormone secretion in domestic fowl: concomitant stimulation of dopamine turnover in the medial basal hypothalamus

1993 ◽  
Vol 138 (2) ◽  
pp. 225-232 ◽  
Author(s):  
S. Harvey ◽  
R. W. Lea
Keyword(s):  
Domestic Fowl ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Extracellular Fluid ◽  
Dopamine Turnover ◽  
Synthesis Inhibitor ◽  
Thyrotrophin Releasing Hormone ◽  
Medial Basal Hypothalamus ◽  
Releasing Hormone

ABSTRACT Thyrotrophin-releasing hormone (TRH) stimulates GH secretion in domestic fowl by actions at pituitary and central nervous system sites. The possibility that this central action might be mediated by hypothalamic catecholamines or indoleamines was therefore investigated. When TRH was administered into the lateral ventricles of anaesthetized fowl the concentration of 3,4-dihydroxyphenylacetic acid (DOPAC, a metabolite of dopamine (DA)) in the medial basal hypothalamus (MBH) was increased within 20 min. The concentrations of MBH noradrenaline (NA), DA, serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were, however, unaffected by the intracerebroventricular (i.c.v.) administration of TRH, although the MBH concentrations of somatostatin and TRH were concomitantly reduced. A rapid increase in DA release into MBH extracellular fluid and its metabolism to DOPAC was also observed after i.c.v. or i.v. administration of TRH, in birds in which the MBH was perfused in vivo with Ringer's solution. Microdialysate concentrations of NA, 5-HT and 5-HIAA were not, however, affected by central or peripheral injections of TRH. Diminished GH responses to i.v. TRH challenge occurred in birds pretreated with reserpine (a catecholamine depletor), α-methyl-paratyrosine (a DA synthesis inhibitor) and pimozide (a DA receptor antagonist). These results therefore provide evidence for the involvement of a hypothalamic dopaminergic pathway in the induction of GH release following the central or peripheral administration of TRH. In contrast with its inhibitory actions at peripheral sites, DA would appear to have a central stimulatory role in regulating GH release in birds. Journal of Endocrinology (1993) 138, 225–232

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
Keyword(s):  
Growth Hormone ◽  
Domestic Fowl ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Growth Hormone Secretion ◽  
Central Effect ◽  
Central Action ◽  
Thyrotrophin Releasing Hormone ◽  
Gh Secretion ◽  
Peripheral Plasma

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

Thyrotrophin-releasing hormone-induced growth hormone (GH) secretion in anaesthetized chickens: inhibition by GH-releasing factor at central sites

1991 ◽  
Vol 128 (1) ◽  
pp. 13-19 ◽  
Author(s):  
C. A. Ahene ◽  
R. W. Lea ◽  
S. Harvey
Keyword(s):  
Domestic Fowl ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Central Effects ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Peripheral Plasma ◽  
Hypothalamic Tissue ◽  
Hypothalamic Function

ABSTRACT Intracerebroventricular (i.c.v.) administration of GH-releasing factor (GRF) (at 1 or 10 μg) to anaesthetized immature (6- to 8-weeks-old) or adult (> 24-weeks-old) domestic fowl had no effect on basal GH concentrations in peripheral plasma, but suppressed (after 20 min) the acute GH response to exogenous (i.v.) thyrotrophin-releasing hormone (TRH) (1 μg/kg). The i.c.v. injection of GRF also reduced the content of somatostatin (SRIF) and dopamine (DA) in the hypothalamus, while increasing the concentration of the DA metabolite 3,4-dihydroxyphenyl acetic acid (DOPAC) and the DOPAC/DA ratio. The release of SRIF from hypothalamic tissue was stimulated in vitro by 100 nmol GRF/l. The inhibitory effect of i.c.v. GRF on TRH-induced GH secretion was blocked when it was simultaneously injected i.c.v. with SRIF antiserum. These results demonstrate central effects of GRF on avian hypothalamic function and suggest an inhibitory role for this peptide in GH regulation, possibly mediated through increased SRIF secretion. Journal of Endocrinology (1991) 128, 13–19

Thyroid hormones inhibit growth hormone secretion in domestic fowl (Gallus domesticus)

1983 ◽  
Vol 96 (2) ◽  
pp. 329-334 ◽  
Author(s):  
S. Harvey
Keyword(s):  
Domestic Fowl ◽  
Single Injection ◽  
Mammalian Species ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Similar Reduction ◽  
Thyrotrophin Releasing Hormone ◽  
Gh Secretion ◽  
Basal Plasma ◽  
Plasma Gh

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.

Thyroidal inhibition of growth hormone secretion in fowl: tri-iodothyronine-induced down-regulation of thyrotrophin-releasing hormone-binding sites on pituitary membranes

1990 ◽  
Vol 4 (2) ◽  
pp. 127-134 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan
Keyword(s):  
Binding Sites ◽  
Plasma Membranes ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Down Regulation ◽  
Thyrotrophin Releasing Hormone ◽  
Caudal Lobe ◽  
Gh Secretion

ABSTRACT The number, but not affinity, of binding sites for [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) on chicken adenohypophysial plasma membranes was increased in chickens made hypothyroid by goitrogen (methimazole) treatment (50 mg/kg per day for 7 days), which also increased circulating GH concentrations. Daily i.p. injection of thyroxine (T4; 100 μg/kg for 7 days) had no effect on [3H]Me-TRH binding to pituitary membranes, although it suppressed endogenous GH secretion. Binding of [3H]Me-TRH to pituitary caudal lobe membranes was, however, suppressed by tri-iodothyronine (T3) injected chronically (100 μg/kg per day, i.p., for 7 days) or acutely (100 μg/kg, 2 h before being killed). The suppression of [3H]Me-TRH binding and inhibition of GH secretion following T3 administration was dose related. Binding of [3H]Me-TRH to caudal lobe membranes was also suppressed following the incubation of pituitary glands with T3 in vitro, and the response was both dose and time related. These results suggest that T3 inhibits GH secretion in fowl by a down-regulation of pituitary TRH receptors. However, other mechanisms are involved in thyroidal inhibition of GH release in birds, since T4 had no effects on [3H]Me-TRH binding yet suppressed GH secretion in vivo.

Brain sites involved in the regulation of growth hormone secretion in the young male domestic fowl

1984 ◽  
Vol 103 (3) ◽  
pp. 327-332 ◽  
Author(s):  
J. Rabii ◽  
L. Knapp ◽  
A. De La Guardia ◽  
P. Zafian ◽  
T. J. Lauterio ◽  
...  
Keyword(s):  
Domestic Fowl ◽  
Arcuate Nucleus ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Young Male ◽  
High Concentration ◽  
Gh Secretion ◽  
Regulation Of Growth ◽  
Fair Degree ◽  
Made In

ABSTRACT To study brain sites involved in the regulation of GH secretion in the domestic fowl, lesions were placed in and around the hypothalamus of 1-week-old cockerels. Circulating concentrations of GH were then measured at weekly intervals for 4 weeks after the placement of lesions. At the termination of the experiment, histological procedures were used to determine the exact site of the lesion in each bird. Although a fair degree of overlap existed between the lesion sites leading to stimulation and those causing an inhibition of GH secretion, a clear distinction could be made in the overall distribution of stimulatory and inhibitory sites of GH control. A high concentration of lesion sites resulting in GH decline (presumed GH-releasing factor-rich areas) appeared to reside in the general area of the ventromedial and the arcuate nucleus of the hypothalamus. Lesion sites causing a GH rise (presumed somatostatin-rich areas), on the other hand, seemed to have a more caudal distribution. In addition, some evidence of an anterior hypothalamic distribution of these presumed 'somatostatin' neurones was observed. These agree with the existing immunohistochemical data on the distribution of somatostatin and constitute experimental evidence for localization of presumed GH-releasing factor sites within the avian brain. J. Endocr. (1984) 103, 327–332

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