Short-loop inhibition of thyrotrophin-releasing hormone-induced growth hormone secretion in fowl

1990 ◽  
Vol 126 (2) ◽  
pp. 237-244 ◽  
Author(s):  
R. W. Lea ◽  
C. A. Ahene ◽  
J. A. Marsh ◽  
S. Harvey
Keyword(s):  
Growth Hormone ◽  
Bovine Serum Albumin ◽  
Binding Sites ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Medial Basal Hypothalamus ◽  
Short Loop ◽  
Basal Plasma ◽  
Plasma Gh

ABSTRACT The i.c.v. administration of 0·1 or 10 μg ovine (o)GH to 12- to 16-week-old hypothyroid chickens of a sex-linked dwarf (SLD) strain suppressed the basal plasma GH concentrations, measured 24 h afterwards. The GH response of the oGH-injected SLDs to TRH was suppressed, in a dose-related way, in comparison with that induced by TRH in birds given control injections (10 μg) of bovine serum albumin (BSA). Basal circulating concentrations of GH in euthyroid K strain birds of the same age were even lower than in the SLDs following injection of 10 μg oGH, and were not further reduced by oGH administration. The GH response to TRH in the K strain birds injected i.c.v. with 0·1 or 10 μg oGH was, nevertheless, suppressed in comparison with the BSA-injected K strain controls. The i.c.v. administration of oGH also suppressed circulating concentrations of LH and the LH response to TRH in the K strain birds. Twenty-four hours after i.c.v. administration of oGH (10 μg), the somatostatin (SRIF) content in the medial basal hypothalamus of 8-week-old euthyroid cockerels was greater than that in BSA (10 μg)-injected controls. At the same time, the binding of [3H]3-methyl-histidine2-TRH to the pituitary caudal and cephalic lobes of GH-injected birds was less than that in the controls. These results suggest that GH regulation in avian species is partly mediated by an inhibitory short-loop mechanism (mediated by hypothalamic SRIF and a down-regulation of pituitary TRH-binding sites) that suppresses basal and secretagogue-induced GH release. Journal of Endocrinology (1990) 126, 237–244

Somatostatin tonically inhibits growth hormone secretion in domestic fowl

1986 ◽  
Vol 111 (1) ◽  
pp. 91-97 ◽  
Author(s):  
S. Harvey ◽  
S.-K. Lam ◽  
T. R. Hall
Keyword(s):  
Growth Hormone ◽  
Domestic Fowl ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Passive Immunization ◽  
Inhibitory Effect ◽  
Gh Secretion ◽  
Basal Plasma ◽  
Plasma Gh

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

CHLORPROMAZINE INHIBITS EPISODIC GROWTH HORMONE SECRETION IN THE RAT

1979 ◽  
Vol 91 (3) ◽  
pp. 428-436 ◽  
Author(s):  
Ichiji Wakabayashi ◽  
Megumi Kanda ◽  
Nobuyasu Miki ◽  
Reiko Demura ◽  
Kazuo Shizume
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Right Atrial ◽  
Plasma Prolactin ◽  
Medial Basal Hypothalamus ◽  
Conscious Rats ◽  
Gh Secretion ◽  
Episodic Growth ◽  
Plasma Gh

ABSTRACT Effects of chlorpromazine (CPZ) on plasma GH and prolactin levels were observed in conscious rats provided with chronic indwelling right atrial cannulae. The administration of CPZ (200 μg/100 g b.w. iv) suppressed episodic plasma GH burst and resulted in significant elevations of plasma prolactin levels. These were also observed in rats in which two types of hypothalamic deafferentation, i.e. anterior and complete, had been carried out. The data suggest that CPZ acts within the medial basal hypothalamus and inhibits episodic plasma GH secretion. In addition, it is inferred that catecholamines are involved in the generation of episodic plasma GH burst.

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.

Lack of episodic growth hormone secretion in rats with anterolateral deafferentation of the medial-basal hypothalamus

1982 ◽  
Vol 94 (1) ◽  
pp. 77-81 ◽  
Author(s):  
M. Kárteszi ◽  
J. Fiók ◽  
G. B. Makara
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Right Atrial ◽  
Neural Pathways ◽  
Time Intervals ◽  
Medial Basal Hypothalamus ◽  
Episodic Growth ◽  
Postoperative Time ◽  
Plasma Gh

Growth hormone secretory dynamics were studied in rats sampled through chronic indwelling right atrial cannulae at time-intervals ranging from 2 days to 2 months after placing an anterolateral cut (ALC) around the medial-basal hypothalamus (MBH). The episodic secretion normally occurring in the control animals could not be seen in the rats with an ALC. Instead of the usual high bursts and low trough levels occurring between 09.00 and 13.00 h in the controls, the operated animals had fairly constant plasma GH levels with only minor fluctuations at all postoperative time-points studied. These results suggest that (1) the isolated MBH is incapable of maintaining the episodic secretion of GH and (2) the pulsatile hormone release is dependent on neural pathways entering the MBH from an anterolateral direction.

Desensitization of thyrotrophin-releasing hormone (TRH)-induced growth hormone secretion in chickens: coincident down-regulation of TRH binding to pituitary membranes

1990 ◽  
Vol 4 (3) ◽  
pp. 223-230 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan
Keyword(s):  
Growth Hormone ◽  
Binding Sites ◽  
Plasma Membranes ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Down Regulation ◽  
Thyrotrophin Releasing Hormone ◽  
Caudal Lobe

ABSTRACT Release of GH is stimulated by TRH in chickens. However, for 60 min following a priming injection of TRH, a second injection of TRH is unable to provoke further GH release. TRH binds to the plasma membranes of the pituitary caudal lobe, in which somatotrophs predominate, although the magnitude of [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) binding was reduced (by 25–50%) 30 min after the i.v. administration of a dose of TRH (5 μg/kg maximally effective in provoking GH release. A significant reduction in [3H]Me-TRH binding to caudal lobe membranes was also observed within 15 min of TRH administration and was maintained for at least 60 min. Control levels of [3H]Me-TRH binding were restored 2 h after TRH injection, coincident with the restoration of GH responsiveness to TRH challenge. The suppression of [3H]Me-TRH binding to pituitary membranes 30 min after in-vivo TRH administration was dose related, whereas the maximal (10 min) GH response to TRH was biphasic. The suppression of [3H]Me-TRH binding to chicken pituitary membranes was due to direct pituitary actions of TRH and could be induced by a 30-min exposure to 100 nm TRH in vitro. These results demonstrate that avian pituitary TRH-binding sites differ greatly from mammalian ones in the timing of the onset and duration of down-regulation. Pituitary TRH-binding sites in birds are rapidly and transiently down-regulated following TRH administration in vivo, coincident with the period of GH refractoriness to TRH challenge.

Neuroanatomic localization of the inhibitory effect of TRH on growth hormone secretion

1987 ◽  
Vol 253 (4) ◽  
pp. E354-E359
Author(s):  
K. Ishikawa ◽  
H. Katakami ◽  
L. A. Frohman
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Inhibitory Effect ◽  
Releasing Hormone ◽  
Hypothalamic Deafferentation ◽  
Electrolytic Lesions ◽  
Plasma Gh ◽  
The Right ◽  
Lateral Cerebral Ventricle

The inhibitory effect of centrally administered thyrotropin-releasing hormone (TRH) on the plasma growth hormone (GH) response to GH-releasing hormone (GHRH) in the rat was studied in relation to the anatomic loci involved. Experiments were performed in animals with bilateral electrolytic lesions in the medial preoptic (MPO) area or with anterolateral hypothalamic deafferentation and in sham-operated controls. Blood samples were obtained every 10 to 20 min from and drugs were injected into freely moving animals with indwelling cannulas in the right atrium and lateral cerebral ventricle. In control animals, the plasma GH response to GHRH, 1 microgram iv, was almost completely inhibited by TRH, 1 microgram icv, injected 5 min previously. In animals with either MPO lesions or anterolateral hypothalamic deafferentation in which median eminence somatostatin immunochemical staining was almost completely eliminated, the GH response to GHRH was enhanced and TRH did not exhibit any inhibitory effect. These results, together with the previous observation that the inhibitory effect of TRH is blocked by prior treatment with anti-somatostatin serum, suggest that the effect of TRH is mediated by stimulation of somatostatin-containing neurons in the periventricular nucleus of the MPO area.

Effect of actively immunizing sheep against growth hormone-releasing hormone or somatostatin on spontaneous pulsatile and neostigmine-induced growth hormone secretion

1995 ◽  
Vol 144 (1) ◽  
pp. 83-90 ◽  
Author(s):  
E Magnan ◽  
L Mazzocchi ◽  
M Cataldi ◽  
V Guillaume ◽  
A Dutour ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Physiological Role ◽  
Gh Secretion ◽  
Igf I ◽  
Plasma Gh ◽  
Hypophysial Portal

Abstract The physiological role of endogenous circulating GHreleasing hormone (GHRH) and somatostatin (SRIH) on spontaneous pulsatile and neostigmine-induced secretion of GH was investigated in adult rams actively immunized against each neuropeptide. All animals developed antibodies at concentrations sufficient for immunoneutralization of GHRH and SRIH levels in hypophysial portal blood. In the anti GHRH group, plasma GH levels were very low; the amplitude of GH pulses was strikingly reduced, although their number was unchanged. No stimulation of GH release was observed after neostigmine administration. The reduction of GH secretion was associated with a decreased body weight and a significant reduction in plasma IGF-I concentration. In the antiSRIH group, no changes in basal and pulsatile GH secretion or the GH response to neostigmine were observed as compared to controls. Body weight was not significantly altered and plasma IGF-I levels were reduced in these animals. These results suggest that in sheep, circulating SRIH (in the systemic and hypophysial portal vasculature) does not play a significant role in pulsatile and neostigmine-induced secretion of GH. The mechanisms of its influence on body weight and production of IGF-I remain to be determined. Journal of Endocrinology (1995) 144, 83–90

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