1. The turnovers of hypothalamic 5-hydroxytryptamine (5HT), dopamine (DA) and noradrenaline (NE) were measured in male and female ring doves (Streptopelia risoria) at three stages of the breeding cycle: courtship, 3 days after pairing; early incubation, 1-2 days after egg laying; and brooding, 1-3 days after the squabs had hatched.2. In both sexes plasma LH decreased progressively from courtship through incubation to brooding young. Crop sacs were fully developed in doves brooding young but not at other stages of the reproductive cycle, indicating increased concentrations of plasma prolactin.3. The turnovers of 5HT and DA in both sexes were significantly higher (P < 0.001) in doves brooding young than in birds incubating eggs or nest building. The turnover of DA was higher in females than in males at the onset of incubation. The turnover of NE was lower (P > 0.01) in females at the onset of incubation than during courtship or brooding.4. Increased turnover of hypothalamic DA may be more closely related to brooding behaviour than to changes in prolactin or LH secretion.5. Increased hypothalamic 5HT turnover in brooding doves appears to be more directly related to crop sac development, and by inference increased prolactin secretion, than to depressed plasma LH concentrations.

The concentration of plasma triiodothyronine (T3), thyroxine (T4), corticosterone, and glucose as well as body weight and food intake were measured in pairs of ring doves throughout a breeding cycle and during food deprivation. During courtship and incubation the levels of plasma T4 were significantly higher in males than in females. A transitory decrease in food intake in both sexes was measured at the onset of incubation but was not associated with a change in body weight or in levels of plasma thyroid hormones. After the eggs had hatched, food intake increased but was associated with a reduction in body weight and concentrations of plasma T3 and T4, although plasma corticosterone and glucose both increased. Food deprivation for 48 hr resulted in a significant fall in the concentration of plasma T3 and an increase in plasma corticosterone. These changes suggest that all the food was not being digested by the adult birds during brooding but was almost exclusively regurgitated to feed the squabs.

Galanin is a 29-amino acid neuroactive peptide, first isolated from porcine intestine, but subsequently shown to possess a broad range of biological actions in mammals and at least one avian species. High concentrations of galanin-like reactivity have been detected in the central nervous system, particularly hypothalamus, of species as diverse as rats and sea bass (Holland Cheung 1990). Galanin is known to stimulate release of GH in several mammals, including human and rat, as well as in the chicken, but it is much more potent in combination with GH releasing hormone (GHRH) {Cheung and Hall 1990; Hall and Cheung 1990). The peptide also stimulates the release of prolactin, probably through stimulation of hypothalamic vasoactive intestinal peptide release (Inoue, Kato, Koshiyama, Yanaihara and Imura 1989). In the rat brain, a certain number of galanin-reactive neurones also contain LH releasing hormone (LHRH), particularly in the preoptic region, several galanin-containing neurones terminate on LHRH neurones, and galanin can stimulate the release of LHRH from nerve terminals of the median eminence in vitro (Merchenthaler, Lopez and Negro-Vilar 1990). Lopez, Merchenthaler, Ching, Wisniewski and Negro-Vilar (1990) also demonstrated that galanin and LHRH are secreted in a coincident manner into the portal circulation, and that galanin stimulates LH release and potentiates the actions of LHRH on dispersed pituitary cells. In the present study we examined the actions of galanin in vitro and in vivo on LH release in young broiler chickens.

Galanin, a novel peptide originally isolated from porcine intestine, has a wide distribution in the nervous system and is known to enhance the release of growth hormone in mammals, though the mechanism of its actions is still subject to debate. In the current study, the effects of galanin on growth hormone secretion in the domestic fowl were investigated. Intravenous injections of galanin into both 8‐week old and 18‐week old female Hubbard broilers produced marked increases in plasma growth hormone, similar in magnitude to that evoked by human growth hormone‐releasing factor. Galanin produced dose‐related increases in growth hormone release, with a peak response occurring within 10 min of administration. Growth hormone release in response to a maximal challenge of growth hormone‐releasing factor was further augmented when galanin was given at the same time. Galanin stimulated growth hormone release from chick hemipituitary glands in vitro , a response which was not dependent upon hypothalamic input. In addition, galanin potentiated the actions of growth hormone‐releasing factor on growth hormone release in vitro and these responses were reversed by somatostatin. These results show that galanin is able to stimulate growth hormone release in the domestic fowl by acting directly on the pituitary gland.

Young cockerels (6-8 weeks old) were injected with serum from sheep immunized against somatostatin-14 (anti-SRIF) or normal sheep serum (NSS). Blood samples were withdrawn periodically for the determination of plasma corticosterone concentration by radioimmunoassay. With frequent (every 10 min) sampling, NSS-treated control animals exhibited increased plasma corticosterone levels, presumably as a stress response to the experimental manipulation. Anti-SRIF stimulated a much greater increase in plasma corticosterone concentrations and a peak response was observed within 10 to 20 min, when the plasma corticosterone level reached more than twice that of the corresponding control value. With less frequent sampling, plasma corticosterone increased with anti-SRIF administration to as much as nine times the corresponding control value, and the peak response occurred much later. Under pentobarbitone anaesthesia, which itself increased basal corticosterone concentrations, anti-SRIF treatment promoted further increases in plasma corticosterone levels although to a smaller magnitude compared with conscious birds. The results suggest that endogenous somatostatin may play a role in the regulation of adrenocortical function in the domestic fowl. The mechanism of response may involve a central component.

The effects of recombinant DNA-derived chicken growth hormone (rcGH) on plasma corticosterone in young broiler cockerels were investigated. A single injection of 200 μg/kg rcGH significantly increased plasma corticosterone concentrations 2 hr (but not 20 or 40 min) after treatment. Administration of 10 or 100 μg/kg rcGH also significantly increased plasma corticosterone levels after 2 hr, with the higher dose eliciting greater responses. Chronic treatment with seven daily injections of the same doses of rcGH gave similar increases in plasma concentrations of corticosterone. No obvious difference in magnitude of plasma corticosterone was observed between acute and chronic exposure to rcGH. In a further experiment in which serial blood sampling was performed after a single injection or five daily injections of vehicle or 200 μg/kg rcGH, there were significant increases in plasma corticosterone concentrations 40 min after acute rcGH treatment and 40 and 80 min after chronic treatment when compared with plasma corticosterone concentrations of vehicle-injected controls. However, the increases could have incorporated a stress response due to repeated sampling because the control birds also showed elevated plasma corticosterone concentrations. The corticosterone response did not diminish with repeated GH challenge. These results suggest that GH may play a role in the acute regulation of corticosterone secretion in intact chickens.

Sodium pentabarbitone anaesthesia lowered the circulating growth hormone (GH) concentration in immature chickens and reduced basal and stimulated pituitary GH release in vitro. The immunoneutralization of endogenous somatostatin (SRIF), by passive SRIF immunization, overcame the inhibitory effect of anaesthesia on basal GH secretion in vivo, but had no direct effects on GH release in vitro. However, while SRIF immunization restored the resting GH concentration in the anaesthetized birds, it increased greatly the GH level in conscious birds. These results therefore suggest that the inhibition of GH secretion in anaesthetized birds may be partly SRIF-mediated, although a suppression of hypothalamic stimulation may also be involved.

The effects of serotoninergic drugs on adrenocortical function in domestic fowl were examined. Administration of the serotonin receptor agonist 2-(1-piperazinyl)quinoline maleate (quipazine), an inhibitor of serotonin metabolism, N-methyl-N-2-propynylbenzylamine HCl (pargyline), as well as serotonin itself, all increased plasma concentrations of corticosterone. The maximum responses to serotonin and quipazine occurred 1 h after treatment. The quipazine-stimulated response was partly prevented by the serotonin antagonist cyproheptadine. Cockerels pretreated with dexamethasone, a synthetic steroid known to inhibit pituitary ACTH release, showed attenuated responses to subsequent quipazine, pargyline or serotonin injection. Serotonin, quipazine and cyproheptadine did not affect corticosterone release directly from the adrenal gland incubated in vitro, nor did they affect adrenal responsiveness to ACTH stimulation. The neurotoxin 5,6-dihydroxytryptamine injected into day-old chicks decreased plasma concentrations of corticosterone for up to 7 days after treatment, with corresponding decreases in the hypothalamic concentration of serotonin, but not dopamine or noradrenaline concentrations. These results show that adrenal corticosterone secretion is regulated by a central serotoninergic system, probably acting on the hypothalamo-pituitary-adrenal axis.

The effects of the calcium antagonists ethyleneglycol-bis-(beta-aminoethylether)-N,N,N',N'-tetraace tic acid (EGTA), cobalt chloride (CoCl2), and magnesium chloride (MgCl2) on the concentrations of plasma thyroxine (T4) and triiodothyronine (T3) and on the basal and stimulated release of T4 from incubated thyroid glands have been determined in the domestic fowl. Plasma T4 levels were consistently reduced 2 hr after the administration of each calcium antagonist, although only EGTA and CoCl2 lowered the concentration of plasma total calcium. Concentrations of plasma T3 were increased following MgCl2 treatment but reduced after CoCl2 administration. The basal release of T4 by incubated thyroid glands was reduced following in vivo EGTA and CoCl2 treatment, but increased after MgCl2 injection. The addition of bovine thyroid stimulating hormone (TSH, 200 mU) to the incubation consistently stimulated in vitro T4 release, although the magnitude of the stimulation was increased following in vivo EGTA or CoCl2 treatment and reduced after MgCl2 administration. These results demonstrate the involvement of calcium dependent mechanisms in the control of T4 release in fowl.

A method for measuring the concentration and turnover of serotonin, dopamine and noradrenaline in small amounts of brain tissue was validated for the ring dove (Streptopelia risoria). Turnover rates of the catecholamines calculated as the rate of depletion after tyrosine hydroxylase inhibition agreed well with turnover rate measured as rate of accumulation after inhibition of monoamine oxidase at 2.5 h, but not 5 h, after drug administration. Using the monoamine oxidase inhibitor, pargyline, turnover of serotonin, dopamine and noradrenaline were estimated in the same tissue. Both the concentration and turnover of the amines in hypothalamus, paleostriatum and hyperstriatum fluctuated over a 24 h period. Serotonin turnover was greatest during the middle of the dark period in all three tissues. In contrast, for both dopamine and noradrenaline the highest turnover was observed during the light period and the lowest during the dark period.

Immunoneutralization of endogenous somatostatin (SRIF)-28(1-14) by the intravenous or intramuscular administration of a specific antiserum promptly enhanced the growth hormone (GH) concentration in the plasma of 4 to 8-week-old cockerels. The magnitude of the GH response was related to the volume of antiserum administered. The release of GH from chicken pituitary glands incubated with intact hypothalami was increased in the presence of anti-SRIF-28(1-14). These results suggest that SRIF-28(1-14)-like peptides are physiologically involved in the control of GH secretion in chickens, in which they may tonically inhibit GH release.

The biological activity of recombinant-DNA-derived chicken growth hormone (rcGH) has been examined in young broiler cockerels, by determining its effects on plasma concentrations of glucose, free fatty acids and alpha-amino nitrogen. A single injection of rcGH increased plasma glucose, which remained high for several hours, whereas daily treatment with rcGH for 1 week had no effect on basal plasma glucose concentrations but blunted the glucose response to a further rcGH challenge. Plasma free fatty acids were also promptly increased following acute rcGH treatment, and chronic exposure to rcGH again attenuated this response. The effects of rcGH on plasma alpha-amino nitrogen were more variable. The stress of repeated blood sampling tended to reduce alpha-amino nitrogen, and after rcGH, an increase relative to vehicle-injected controls was seen in both acute and chronically-treated birds. These data suggest that rcGH has both hyperglycaemic and lipolytic activity in chickens, and may also increase amino acid availability.

Basal and thyrotrophin (TSH)-stimulated release of iodothyronines (triiodothyronine, T3, and thyroxine, T4) from intact chicken thyroid glands was determined in vitro. In the absence of TSH, T3 and T4 were released in measurable amounts in the incubation media. The release of both iodothyronines was directly related to the media TSH concentrations and incubation period. Lineweaver-Burke analysis revealed that the Vmax for T3 was 99.4 pg/gland, with an apparent Km of 17.8 mU TSH, and that the Vmax for T4 was 323.35 ng/gland, with an apparent Km of 51.5 mU TSH, demonstrating that T4 is the major iodothyronine released by avian thyroid glands. The basal release of T4 was suppressed by the addition of a calcium chelator (ethyleneglycol-bis-(beta-aminoethylether)-N,N,N', N'-tetraacetic acid; EGTA), a calcium antagonist (cobalt chloride, CoCl2), or prostaglandin E1 (PGE1) to the incubation media. Basal T4 released was increased in the presence of a calcium agonist (lanthanum chloride, LaCl3), a calcium ionophore (A23187), dibutyryl cyclic adenosine 3'3'-monophosphate (dbcAMP), isobutylmethylxanthine (IBMX), indomethacin, magnesium chloride (MgCl2), and potassium iodide (KI). Thyrotrophin-stimulated T4 release was reduced by CoCl2, PGE1, and indomethacin but enhanced by LaCl3, MgCl2, and KI. These results demonstrate that it is possible to measure the release of thyroid hormones in an in vitro system in the chicken. Basal and stimulated iodothyronine release from the chicken thyroid gland appears to be mediated by calcium- and cAMP-dependent mechanisms.

Dopamine beta-hydroxylase (DβH) plays an essential role in the synthesis of catecholamines (CA) in neuroendocrine networks. In the razor clam, Sinonovacula constricta a novel gene for DβH (ScDβH-α) was identified that belongs to the copper type II ascorbate-dependent monooxygenase family. Expression analysis revealed ScDβH-α gene transcripts were abundant in the liver and expressed throughout development. Knock-down of ScDβH-α in adult clams using siRNA caused a reduction in the growth rate compared to control clams. Reduced growth was associated with strong down-regulation of gene transcripts for the growth-related factors, platelet derived growth factors A (PDGF-A) (P < 0.001) 24 h after ScDβH-α knock-down, vascular endothelial growth factor (VEGF1) (P < 0.001) and platelet derived growth factor B (PDGF-B-2) (P < 0.001) 24 h and 48 h after ScDβH-α knock-down and transforming growth factor beta (TGF-β1) (P < 0.001) 48 h and 72 h after ScDβH-α knock-down. Taken together the results suggest that the novel ScDβH-α gene through its role in CA synthesis is involved in growth regulation in the razor clam and possibly other bivalves.

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.

Monoamine oxidase (MAO) activity was determined fluorometrically in brain, intestine, kidney and liver tissues of the rainbow trout, Salmo gairdneri. MAO activity was inhibited by various drugs in a concentration-related manner, with single sigmoid inhibition curves, the inhibitors of type A MAO, harmaline and clorgyline being more effective than deprenyl, an inhibitor of type B MAO. Intestine exhibited greatest MAO activity followed by liver and brain with kidney showing least activity. The Michaelis constants (Km) also showed variability between tissues. Inhibition of MAO by harmaline was non-competitive and dependent on the concentration of substrate present.