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Biomedical subjects

T R Hall

Publications and source records attributed to T R Hall.

At least 91 records · Page 5Linked to original sources
PubMed1984

Neurotransmitter effects on in vitro prolactin and growth hormone release from fowl pituitary glands: dopamine and noradrenaline.

Pituitary glands and hypothalami from broiler fowl heads were incubated alone or together with dopamine, noradrenaline or monoaminergic drugs (apomorphine, pimozide, phentolamine, isoproterenol and propranolol). The basal release of both prolactin and growth hormone was not affected by any of these amines or aminergic drugs. The co-incubation of pituitary glands with whole hypothalami consistently stimulated prolactin and growth hormone secretion. Apomorphine inhibited hypothalamus-induced prolactin and growth hormone release and the response was blocked by pimozide. Noradrenaline markedly stimulated hypothalamus-induced prolactin release, an effect antagonised by phentolamine. Thyrotrophin-releasing hormone (TRH) stimulated the release of prolactin and this stimulation was reversed, in a dose-related manner, by dopamine. TRH also increased the release of growth hormone, in the presence or absence of dopamine. These results demonstrate inhibitory dopaminergic effects on prolactin and growth hormone secretion and stimulatory noradrenergic effects on prolactin release. These aminergic effects may be mediated at pituitary and/or hypothalamic sites.

Animals↗
PubMed1984

Effects of reserpine on recovery rates after inhibition of monoamine oxidase in different regions of mouse brain.

Adult mice were injected once with the monoamine oxidase (MAO) inhibitor pargyline, every 3 days with the amine storage depletor reserpine, or with both drugs. Serotonin content of brainstem and cerebrum was increased after pargyline, decreased after reserpine, and showed intermediate values following administration of both drugs. MAO activity after pargyline recovered in a time-dependent fashion, with recovery rates of hypothalamus greater than cerebellum greater than cerebrum greater than brainstem. After reserpine, recovery rates of MAO were less in hypothalamus and cerebellum, suggesting that the amount of MAO synthesized may be related to the level of substrates in these regions.

Animals↗
PubMed1984

Effects of clomiphene citrate, a nonsteroidal antiestrogen, on brain monoaminergic mechanisms in female goldfish, Carassius auratus.

The antiestrogen, clomiphene citrate ( Merrell -National Laboratories) was administered to female goldfish in order to test the hypothesis that this drug may act on brain monoaminergic mechanisms. Brain monoamine oxidase (MAO) activity and hypothalamic serotonin (5-HT) content were measured fluorometrically after i.p. administration of 0, 5 or 25 micrograms clomiphene citrate/g body wt. Brain MAO activity was significantly inhibited by the high dose of clomiphene citrate, whereas hypothalamic 5-HT content was significantly elevated by both low and high doses of the antiestrogen. These data support the idea that brain monoamines in teleost fish are influenced by estrogen feedback mechanisms which can be blocked by clomiphene citrate.

Animals↗
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

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

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

Effects of synthetic mammalian thyrotrophin releasing hormone, somatostatin and dopamine on the secretion of prolactin and growth hormone from amphibian and reptilian pituitary glands incubated in vitro.

Pituitary glands of grassfrog (Rana pipiens), bullfrog (Rana catesbeiana), clawed toad (Xenopus laevis) and two species of terrapin (Chrysemys picta and Pseudemys scripta) were incubated in medium containing hypothalamic extract (HE), thyrotrophin releasing hormone (TRH), somatostatin, dopamine, or combinations of these treatments. Prolactin and GH concentrations in the medium were determined by densitometry after polyacrylamide-gel electrophoretic separation. Hypothalamic extract stimulated secretion of both hormones in all species tested. Thyrotrophin releasing hormone stimulated secretion of prolactin and GH, showing a biphasic pattern of response. Dopamine had little effect alone, but inhibited HE- and TRH-stimulated release of prolactin, but not GH, in both amphibia and reptiles. Somatostatin by itself had no apparent effect on release of hormones, but it inhibited HE- and TRH-stimulated release of GH from both amphibian and reptilian pituitary glands. These results indicate that factors affecting mammals and birds also interact in the regulation of secretion of prolactin and GH in lower vertebrate species.

Animals↗
PubMed1984

Effect of dehydration, haemorrhage and oviposition on serum concentrations of vasotocin, mesotocin and prolactin in the chicken.

Serum concentrations of arginine vasotocin (AVT), mesotocin and prolactin were determined by radioimmunoassay in Rhode Island Red chickens during and after dehydration, haemorrhage and oviposition. During dehydration increased circulating levels of AVT, mesotocin and prolactin were found. As water deprivation proceeded, marked differences were observed. After an initial rise in serum AVT, mesotocin and prolactin levels during mild and moderate dehydration, concentrations of both AVT and prolactin tended to normalize during continued water deprivation, while those of mesotocin remained high throughout the whole dehydration experiment with the highest at the end of the water-deprivation period. Removal of 5 ml blood at intervals of 10 min during six consecutive time-periods did not affect serum osmolality and circulating levels of AVT and prolactin, but slightly increased mesotocin. These results suggest an osmoregulatory role for AVT and prolactin, whereas mesotocin may be involved in volume control. Finally, 1 min after oviposition, control values of 19.5 +/- 3.4 pmol AVT/1 (n = 9) were raised more than sevenfold to 142.9 +/- 12.5 pmol/l (n = 11). Thereafter, a decline occurred with a half-life for AVT of 13 min with raised serum levels up to 31 min after oviposition. In contrast, the serum concentrations of mesotocin and prolactin remained unaffected by oviposition.

Animals↗
PubMed1984

Dopaminergic inhibition of prolactin release from pituitary glands of the domestic fowl incubated in vitro.

Anterior pituitary glands from broiler fowl were incubated by themselves, with hypothalamic tissue or with thyrotrophin releasing hormone (TRH) in medium containing dopamine and its antagonist pimozide. The presence of hypothalamic tissue or TRH resulted in a stimulation of release of prolactin. Neither dopamine nor pimozide affected prolactin release directly from the pituitary gland. Dopamine inhibited the release of prolactin stimulated by hypothalamic tissue or TRH, in a concentration-dependent fashion. Pimozide diminished the response to dopamine. After pituitary glands were preincubated for 20 h in medium containing oestradiol-17 beta, the basal release of prolactin was enhanced as was the response to TRH. Both basal and TRH-stimulated release of prolactin from the oestrogen-primed pituitary glands was inhibited by dopamine, an effect blocked by pimozide. Hypothalami from broiler fowl were incubated for up to 8 h in medium containing dopaminergic drugs and pituitary glands were incubated in this medium, alone or with pimozide. As indicated by the prolactin released by the pituitary glands, the hypothalami appeared to secrete prolactin-releasing activity in a time-related fashion. Dopaminergic activity was also present in the hypothalami, since pimozide enhanced the prolactin-releasing activity of the medium. Dopamine apparently inhibited and pimozide stimulated the secretion of releasing activity from the hypothalamus. These results suggest that dopamine inhibits release of prolactin directly from the pituitary gland only when prolactin secretion is high. The hypothalamus secretes at least two factors regulating prolactin secretion, a prolactin-releasing factor and a dopaminergic prolactin-inhibiting factor. Dopamine may also play an inhibitory role in the regulation of secretion of the prolactin-releasing factor.

Animals↗
PubMed1983

Hypothalamic control of prolactin and growth hormone secretion in the pituitary gland of the pigeon and the chicken: in vitro studies.

Hypothalamic extracts stimulated the release of prolactin and growth hormone from pigeon and chicken pituitary glands incubated in vitro. Release of hormone was proportional to the amount of hypothalamic extract added. Pituitary glands from "lactating" pigeons released more prolactin and their hypothalami contained more prolactin-releasing activity compared with controls. Partial separation of prolactin releasing activity from growth hormone releasing activity in chicken hypothalamic extract was achieved using gel filtration chromatography. Co-incubation studies in vitro with hypothalamic tissue present showed that prolactin release from the pituitary was inhibited and growth hormone release was stimulated when dopamine was added to the medium. The effects of dopamine were blocked by the antagonist pimozide. The possible existence of hypothalamic releasing and inhibiting factors regulating secretion of prolactin and growth hormone is discussed.

Animals↗
PubMed1983

Pharmacology and physiology of monoamine oxidase activity in vertebrates--a comparative study.

Monoamine oxidase (MAO) activity is high in brain, where it regulates neurotransmitter levels, and in the 'detoxifying' organs. Two MAO isoenzymes (A and B) apparently exist in terrestrial tetrapods, but only one form (type A-like) can be detected in teleosts and in aquatic amphibia. MAO activity is regulated by both endogenous (hormones, substrates) and exogenous (daylength, temperature) factors.

Animals↗
PubMed1983

Thermal inactivation of mouse brain monoamine oxidase type A and type B.

Mouse brain monoamine oxidase (MAO) type A and type B were incubated at 54 degrees C and samples removed for up to 60 min, and remaining MAO activity was determined. Total MAO activity, type A activity and type B activity all disappeared, presumably due to thermal denaturation, in a time-dependent fashion. The rate of disappearance of MAO type B was faster than that of type A both at pH 7.4 and at pH 9.2, though both types denatured faster at the higher pH compared to the lower pH.

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

Distribution of monoamine oxidase activity in tissues of the urodeles Ambystoma tigrinum (tiger salamander) and Necturus maculosus (mudpuppy).

1. Monoamine oxidase (MAO) activity was determined fluorometrically in tissues of adult mudpuppies, and pre- (young) and post- (adult) metamorphic tiger salamanders. 2. From responses to specific inhibitors it was determined that 95% activity was MAO type A in all tissues. 3. In young salamanders MAO activity was greater in brain and intestine of males than of females, and was considerably higher in kidney of both sexes and in intestine of males compared to adults. 4. MAO activity was distributed differently in the mudpuppy compared to the salamander. Intestine and liver contained high activity and brain had relatively little MAO activity compared to salamander. 5. The apparent Michaelis constant of MAO activity in the different groups and tissues was generally similar, suggesting a similarity of the MAO molecule.

Aging↗
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↗