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Biomedical subjects

S Harvey

Publications and source records attributed to S Harvey.

At least 271 records · Page 15Linked to original sources
PubMed1984

Progesterone inhibits prolactin and growth hormone release from fowl pituitary glands in vitro.

After preincubation of anterior pituitary glands of broiler fowls for 20 h in either medium alone or medium containing progesterone, their responsiveness to hypothalamic stimulation and to thyrotrophin releasing hormone (TRH) was determined. Following exposure to progesterone the basal rate of release of prolactin was reduced in a concentration-related manner but basal growth hormone release was unaffected. Stimulation of the release of prolactin and growth hormone by both hypothalamic extract and TRH was reduced following incubation with progesterone, and the reduction of the prolactin response to TRH was related to progesterone concentration.

Animals↗
PubMed1984

Mapping and spacer identification of rRNA operons of Salmonella typhimurium.

The rRNA operons of Salmonella typhimurium have been characterized with respect to their map position, orientation, and type of tRNA spacer. One of the seven rrn operons was found to be linked to pheA and another was found to be linked to aroE. This information, together with published information about the other five rrn operons, shows that S. typhimurium and Escherichia coli are essentially identical in terms of the number, the map position, and the orientation of all seven operons. S. typhimurium and E. coli were also similar in that four of the rrn spacer regions code for tRNAGlu2 and three code for tRNAAla1B. However, the two species differed in that rrnD coded for tRNAGlu2 and rrnB coded for tRNAAla1B in S. typhimurium. This is the opposite of the arrangement in E. coli. We have tabulated the coordinates of the BamHI and PstI sites flanking six of the S. typhimurium rrn genes and present revisions for the coordinates of some of the E. coli sites.

Base Sequence↗
PubMed1984

Relationship between hypothalamic serotoninergic activity and prolactin and growth hormone secretion in the domestic cockerel.

Cockerels were injected with drugs which affect brain serotoninergic activity. Concentrations of plasma prolactin and growth hormone have been measured and correlated with hypothalamic serotonin and 5-hydroxyindole acetic acid (5HIAA) levels. Tryptophan concentrations in the brain and the activity of monoamine oxidase (MAO types A and B) were also measured in some studies. The administration of the MAO inhibitor, pargyline, produced dose- and time-related reductions in brain MAO type A and B activities, hypothalamic 5HIAA concentrations and plasma growth hormone levels, but increased the hypothalamic serotonin and plasma prolactin concentrations. Clorgyline administration inhibited MAO type A (but not type B) activity and also increased hypothalamic serotonin and plasma prolactin levels, while reducing hypothalamic 5HIAA and circulating growth hormone concentrations. Deprenyl treatment inhibited MAO type B (but not type A) activity but did not significantly affect serotonin, 5HIAA, prolactin or growth hormone levels. The serotonin precursor, tryptophan, elevated brain tryptophan levels when given systemically. It also increased hypothalamic serotonin in a dose-related manner, increased plasma prolactin and reduced plasma growth hormone concentrations. Pargyline and tryptophan treatments affected hormone levels more markedly in 3-week-old than in 18-week-old cockerels. These results demonstrate a strong relationship between hypothalamic serotoninergic activity, MAO type A activity and the secretion of prolactin and growth hormone in the cockerel.

Animals↗
PubMed1984

Comparative stimulation of growth hormone secretion in anaesthetized chickens by human pancreatic growth hormone-releasing factor (hpGRF) and thyrotrophin-releasing hormone (TRH).

Plasma concentrations of growth hormone (GH) were elevated in anaesthetized male domestic fowl following the intravenous administration of either synthetic human pancreatic GH-releasing factor 1-44 (NH2) (hpGRF) or synthetic thyrotrophin-releasing hormone (TRH). In 6-week-old chicks the plasma GH level was elevated between 5 and 10 min after the injection of hpGRF at doses between 1 and 80 micrograms/kg. The magnitude of the response increased with doses of hpGRF between 1 and 10 micrograms/kg but declined with higher doses. The GH concentration rapidly declined between 10 and 20 min and between 20 and 40 min after injection. The administration of TRH had similar effects on GH secretion, although the responses were greater than with comparable doses of hpGRF, and the most effective dose (1-1.4 micrograms/kg) was less than with hpGRF. In anaesthetized adult cockerels GH secretion was also increased by the administration of hpGRF (1-20 micrograms/kg) or TRH (0.1-80 micrograms/kg) and in both cases the dose-response relationship was biphasic. The maximal response to TRH in adult birds was again greater than that produced by hpGRF although the response was less than that elicited in immature birds and required a higher dose (20 micrograms/kg) of TRH. The optimal dose of hpGRF and the magnitude of the GH response induced in adult birds was comparable with that in immature chicks. These results demonstrate provocative effects of TRH and hpGRF on GH secretion in the domestic fowl. The sensitivity of the GH response to TRH suggests that it may have a physiological role in the hypothalamic control of GH secretion.

Age Factors↗
PubMed1984

Serotonin and acetylcholine affect the release of prolactin and growth hormone from pituitary glands of domestic fowl in vitro in the presence of hypothalamic tissue.

Anterior pituitary glands from broiler fowl were incubated alone or with hypothalamic tissue in medium containing either serotonin or serotoninergic drugs, acetylcholine or cholinergic drugs, and the release of prolactin (Prl) and growth hormone (GH) measured by homologous radioimmunoassays. The neurotransmitters and drugs affected the release of hormones from the pituitary gland only when hypothalamic tissue was also present. Serotonin and its agonist quipazine stimulated the release of Prl and inhibited release of GH in a concentration-related manner. The antagonist methysergide blocked the effects of serotonin and quipazine on Prl. Acetylcholine and its agonist pilocarpine also stimulated release of Prl and inhibited release of GH in a concentration-related manner. Atropine blocked these responses. The results show that serotonin and acetylcholine affect pituitary hormone secretion by acting on the hypothalamus. They may stimulate the secretion of a Prl releasing hormone and somatostatin.

Acetylcholine↗
PubMed1984

Prolactin and growth hormone secretion in chickens: stimulation by histamine and inhibition by gamma-aminobutyric acid.

Anterior pituitary glands from chickens (Gallus domesticus) were incubated with or without single, mediobasal chicken hypothalami in medium containing histamine, alone or together with the antagonist diphenhydramine or in medium containing gamma-aminobutyric acid (GABA), alone or together with the antagonists bicuculline or picrotoxin. The release of prolactin (Prl) and growth hormone (GH) was measured by homologous radioimmunoassay. Histamine had no direct effect on the release of either hormone but stimulated Prl (in a dose-related way) and GH release when anterior pituitary glands were co-incubated with hypothalami. Diphenhydramine also had no direct effect on Prl or GH secretion but blocked the stimulatory effect of histamine on hypothalamus-induced Prl and GH release. When anterior pituitary glands were incubated without hypothalami, GABA, bicuculline and picrotoxin had no effect on the release of Prl or GH. However, GABA inhibited the release of both hormones in a concentration-related manner, when anterior pituitary glands were co-incubated with hypothalami. This inhibition was blocked by both bicuculline and picrotoxin. These results suggest that histamine and GABA may be involved in controlling the secretion of Prl and GH from the avian pituitary gland, possible by modifying the secretion of hypothalamic releasing and/or release-inhibiting hormones.

Animals↗
PubMed1984

Inhibition by testosterone of prolactin and growth hormone release from chicken anterior pituitary glands in vitro.

Pituitary glands and hypothalami from broiler fowl were incubated in medium containing testosterone, and prolactin and GH release were determined. Pituitary glands were also preincubated for 20 h in medium containing testosterone, and then in medium containing various secretagogues. Testosterone inhibited the release of prolactin directly from the pituitary gland in a concentration-related manner. The hypothalamus stimulated the release of prolactin, but by a lesser amount in the presence of testosterone. When pituitary glands were preincubated with testosterone, subsequent release of prolactin was inhibited, except with the highest concentration which stimulated prolactin release. Hypothalamic extract (HE) markedly stimulated prolactin release from control pituitary glands although testosterone-primed glands were less responsive. The stimulation of prolactin release by thyrotrophin releasing hormone (TRH) and prostaglandin E2 (PGE2) was also reduced by preincubation of the pituitary glands with testosterone. Priming with testosterone did not affect the release of GH from pituitary glands alone, but reduced the TRH-, HE- and PGE2-stimulated release of GH. These results demonstrate that testosterone directly inhibits prolactin secretion and reduces the sensitivity of pituitary lactotrophs and somatotrophs to provocative stimuli.

Animals↗
PubMed1984

Hormones and growth in poultry.

The hormonal control of growth in poultry and other species is complex. The available evidence supports the concept that growth hormone and the thyroid hormones are the principal hormones responsible for the attainment of normal growth in the domestic fowl. Other hormones, including somatomedins, epidermal growth hormone, sex steroids, and vitamin D metabolites, are also involved in the control of growth. Considerable study will be required for the elucidation of the exact roles of the various hormones in avian growth.

Adrenal Cortex Hormones↗
PubMed1983

Early changes in the adaptation to a low calcium diet in the chick.

Twelve hours after the diet of 3-week-old chicks was changed from a 1% to a 0.1% concentration of calcium (Ca), the growth rate and circulating levels of growth hormone had fallen while renal 25-hydroxecholecalciferol-24-hydroxylase had risen. The amount of 47Ca incorporated into bone from an injection given 18 h previously was lower than in the control birds. Over the following 2 1/2 days on the low Ca diet, the renal 1-hydroxylase activity rose and the plasma prolactin level fell, but the other parameters moved back toward the control level. It was concluded that early adjustments in hormonal and mineral metabolism counteract the acute effects of a dietary Ca shortage until longer-term adaptive changes begin to compensate for a continuing Ca deficiency. The renal hydroxylase activities were not directly influenced by the level of circulating growth hormone or prolactin.

Adaptation, Physiological↗
PubMed1983

Habituation of the corticosterone response of ducks (Anas platyrhynchos) to daily treadmill exercise.

The habituation of the corticosterone response of ducks to treadmill exercise (1.1 km/hr 0 degrees incline for 60 min) has been determined over a 28-day period. In untrained birds 30 min of treadmill exercise resulted in a marked (P less than 0.001) increase in the basal plasma corticosterone level. After 60 min of exercise the corticosterone concentration remained elevated (P less than 0.001) in comparison with basal and control (nonexercised) levels but was less (P less than 0.01) than that at 30 min. Following exercise the concentration declined to basal levels within 60 min. After 7 days of daily training the peak (30 min) corticosterone response to exercise diminished by greater than 50% and was absent in birds trained for 21 days. This habituation of the corticosterone response may be due to adrenocortical stimulation by pituitary adrenocorticotrophin (ACTH) being reduced. As the stimulatory effect of ACTH administration (8 IU/kg) on corticosterone secretion does not habituate in birds treated daily (for 28 days), the reduced corticosterone response to exercise may be due to decreased ACTH release rather than to a reduction in adrenal ACTH sensitivity.

Adrenocorticotropic Hormone↗
PubMed1983

Concentrations of triiodothyronine, growth hormone, and luteinizing hormone in the plasma of thyroidectomised fowl (Gallus domesticus).

Surgical thyroidectomy increased (P less than 0.05) the basal concentrations of growth hormone (GH) and luteinizing hormone (LH) in the plasma of 10- to 12-week-old domestic fowl. The administration of thyrotrophin releasing hormone (TRH) (100 micrograms, sc) increased (P less than 0.01) the GH concentration in both intact and thyroidectomised birds. The magnitude of the TRH-induced increase in GH level was greater (P less than 0.01) in thyroidectomised birds than in intact controls. Although TRH had no effect on LH secretion in the controls, it induced a small (P less than 0.05) rise in the plasma LH level in thyroidectomised birds. In both the intact and thyroidectomised birds the LH concentration was enhanced (P less than 0.05) following the administration of LH-releasing hormone (LH-RH) (20 micrograms, sc). The increase in the LH level by LH-RH in the thyroidectomised birds was greater (P less than 0.001) than that in the intact controls. Plasma GH concentrations were unaffected by LH-RH treatment. These results suggest that thyroid hormones inhibit the secretion of LH and GH in birds. In thyroidectomised birds low levels of immunoreactive triiodothyronine (T3)-like material were measurable in the circulation, despite the absence of regenerated thyroid tissue. The administration of TRH (100 micrograms, sc) did not enhance the plasma level of this material in thyroidectomised birds, whereas plasma T3 concentrations were enhanced in intact birds following TRH treatment. These results suggest that the T3 immunoreactive substance in thyroidectomised birds is extrathyroidal in origin.

Animals↗
PubMed1983

Serotoninergic drugs affect prolactin and growth hormone secretion in the domestic fowl.

Adult fowl of both sexes injected with the monoamine oxidase inhibitor pargyline showed elevated circulating prolactin concentrations and reduced growth hormone concentrations. Young cockerels injected with the serotonin agonist quipazine and the antagonist methysergide showed responses consistent with a serotoninergic stimulatory control of prolactin. Injection of the serotonin precursor tryptophan and the serotonin re-uptake blocker imipramine resulted in elevated prolactin and reduced growth hormone levels. The similarities and differences in the control of prolactin and growth hormone in birds and mammals were discussed.

Animals↗
PubMed1983

Effect of intermittent feeding on blood plasma growth hormone and prolactin in chickens of a heavy breed.

1. Variations in plasma growth hormone (GH) and prolactin concentrations were determined during growth (at 20, 33, 56 and 83 d of age) in ad libitum (control) and intermittently (alternate days) fed chicks. 2. In each group of birds the concentration of plasma GH was inversely related to age. The mean prolactin concentration was highest in the youngest (20-d-old) birds. 3. The concentration of plasma GH in the intermittently-fed birds deprived of food for 24 h (depleted birds) was significantly higher than that in the controls at 33, 56 and 83 d of age. The mean GH concentration in the intermittently-fed birds 24 h after refeeding (repleted birds) was less than that in the depleted ones. 4. The overall mean concentration of plasma prolactin in the depleted birds was significantly less than that in the control and repleted birds. 5. These results are consistent with the effects of fasting on GH and prolactin secretion and demonstrate that growth retardation in the intermittently-fed birds was not due to impaired GH secretion.

Age Factors↗
PubMed1983

Pharmacological disruption of broodiness in White Rock domestic fowls.

The administration of bromocriptine (CB154) to broody hens (Gallus domesticus) impaired resumption of lay. Resumption of lay was stimulated in broody birds treated with clomiphene citrate (an anti-oestrogen) alone or following CB154 administration. The increased oviposition rate following a single intramuscular injection (21 mg) of clomiphene was long lasting, persisting for at least 16 weeks after treatment. Treatment of broody hens with clomiphene consistently improved (by 4%) the hatchability of the fertile eggs subsequently laid.

Animals↗
PubMed1983

Visual and metabolic stimuli cause adrenocortical suppression in fasted chickens during refeeding.

Concentrations of corticosterone were determined in the plasma of fasted domestic fowl before and at intervals after refeeding. The deprivation of food markedly increased (p less than 0.001) the level of plasma corticosterone. When refed ad libitum the corticosterone concentration declined (by 70%) within 45 min to the level in fed birds and remained at this concentration thereafter. A similar depression in the corticosterone concentration was observed when fasted birds were merely given the sight of the same diet, although the concentration returned to the fasting level within 60 min of food presentation. Refeeding diets with different metabolic energy contents demonstrated that the duration of the feeding-induced adrenocortical suppression was energy related. In fasted birds the presentation of an inert cellulose diet caused a temporary decline in the corticosterone level. In the absence of visual stimuli the administration (by force feeding) of the inert diet had no effect on the corticosterone concentration, whereas force feeding of metabolizable diets still induced adrenocortical suppression. These results demonstrate that adrenocortical suppression occurs in fasted refed birds and both visual and metabolic stimuli are involved in this response.

Adrenal Cortex↗
PubMed1983

Mechanism of serotonin effects on prolactin and growth hormone secretion in domestic fowl.

Brain serotonin levels were increased in immature chickens by ip injection of pargyline (75 mg/kg) and clorgyline (5 mg/kg) and by L-tryptophan (100 mg/kg) and imipramine (10 mg/kg) treatment. These treatments increased the circulating prolactin level and reduced the concentration of plasma growth hormone (GH). Treatment with para-chlorophenylalanine (PCPA, 100 mg/kg) reduced the brain serotonin content and the level of plasma prolactin. Treatment with these drugs in vivo similarly affected the basal level of prolactin release from pituitary glands in vitro, although it did not affect the basal level of GH release. The in vitro responsiveness of the pituitary gland to hypothalamic stimuli eliciting prolactin secretion was increased by in vivo pargyline and combined tryptophan: imipramine treatment but reduced by PCPA administration. The in vitro GH response to hypothalamic stimulation was reduced after the in vivo injection of pargyline, clorgyline and tryptophan: imipramine. The hypothalami from clorgyline and tryptophan: imipramine treated birds induced a greater stimulation of in vitro prolactin secretion from control pituitary glands than hypothalami from controls birds, whereas the GH releasing activity was reduced. These results suggest that serotonin stimulates prolactin secretion in chickens by increasing pituitary responsiveness to hypothalamic releasing factors and by increasing the prolactin releasing activity of the hypothalamus. Serotonin appears to suppress GH secretion by reducing pituitary sensitivity to releasing factors and by reducing hypothalamic GH releasing activity.

Animals↗
PubMed1983

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

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 micrograms/day for 10 days or 250 micrograms/kg for 7 days) or T3 (250 micrograms/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 micrograms/kg) or T4 (250 micrograms/kg). In control birds the concentration of plasma GH was greatly increased (greater than 450 micrograms/l) within 10 min of an i.v. injection of thyrotrophin releasing hormone (TRH; 10 micrograms/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.

Animals↗