Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOWLS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources

Morphology and projections of neurons in Remak's nerve of the domestic fowl revealed by intracellular injection of biocytin.

Micro-injections of biocytin were made into neurons in whole-mount preparations of Remak's nerve of the domestic fowl to visualise the morphology and projections of Remak's neurons. Remak's neurons were classified into four distinct morphological types. Remak type-I and -II neurons had a morphology resembling that of mammalian sympathetic neurons. Type-I neurons (found only in juxta-jejunal ganglia) had numerous primary dendritic processes (8-14) with large dendritic fields and extensive dendritic arborizations. Type-II neurons had 2-9 primary dendritic processes, large dendritic fields and sparse dendritic branching. These were found in similar numbers in juxta-rectal and juxta-jejunal ganglia. Remak type-III neurons were the most numerous cell type of juxta-rectal ganglia. They had small cell somata and short dendritic processes that branched infrequently. Remak type-IV neurons (found only in juxta-jejunal ganglia) had a morphology resembling that of invertebrate neurons in that they possessed a prominent long tapering axon from which most of the numerous long dendritic processes emerged. In juxta-jejunal ganglia, all type-IV and most type-I, -II and -III neurons projected orally, whereas axons of juxta-rectal neurons (types II and III) projected either orally or aborally, or projected directly into a lateral nerve bundle supplying the gut. These regional differences in neuron types and axonal projections suggest that different neural circuits exist between Remak's nerve and the small and large intestine.

Animals↗

Sexual dimorphism of arg-vasotocin gene expressing neurons in the telencephalon and dorsal diencephalon of the domestic fowl. An immunocytochemical and in situ hybridization study.

A strong sex dimorphism in the distribution of immunoreactive arginine-vasotocin (AVT) and AVT mRNA was observed in telencephalic and dorsal diencephalic areas of the domestic fowl using immunocytochemistry and in situ hybridization. Two subgroups of immunoreactive parvocellular perikarya surrounded by dense plexus of immunoreactive fibres were found within the bed nucleus of the stria terminalis and the dorsal part of the diencephalic paraventricular region of males. No signs of immunoreactivity were observed within corresponding regions of the female brain. Instead, in females a few scattered weakly stained perikarya were observed rostrally to the level of the anterior commissure, juxtapositioned to the nucleus accumbens and the floor of the lateral ventricle. The distribution of AVT mRNA containing cell profiles fully confirmed the immunocytochemical findings. Osmotic stress induced by water deprivation for 48 h had no influence on the number of immunoreactive or AVT mRNA containing parvocellular cell bodies. However, it resulted in an increase of immunoreactive cell area in the bed nucleus of the stria terminalis and dorsal diencephalon of 5. 9 and 11.7%, respectively. We suggest that the sexually dimorphic vasotocinergic circuit may be involved in the co-ordination of behavioural and autonomic functions in response to environmental stress.

Animals↗

Fowl adenovirus recombinant expressing VP2 of infectious bursal disease virus induces protective immunity against bursal disease.

The right hand end Nde I fragment 3 (90.8-100 map units) of the fowl adenovirus serotype 10 (FAV-10) was characterised so as to allow the location of an insertion site for recombinant vector construction. Infectious bursal disease virus (IBDV) VP2 gene from the Australian classical strain 002/73, under the control of the FAV-10 major late promoter/leader sequence (MLP/LS) was inserted into a unique Not I site that was generated at 99.5 map units. This recombinant virus was produced without deletion of any portion of the FAV-10 genome. When administered to specific pathogen free (SPF) chickens intravenously, intraperitoneally, subcutaneously or intramuscularly, it was shown that the FAV-10/VP2 recombinant induced a serum VP2 antibody response and protected chickens against challenge with IBDV V877, an intermediate virulent classical strain. Birds were not protected when the recombinant was delivered via the conjunctival sac.

Animals↗

Taste sensitivity in the embryo of the domestic fowl.

Two experiments were carried out to investigate the sense of taste in embryos of the domestic fowl. In the first, four taste substances; NaCl, HCl, glucose and SOA were diluted with distilled water and the response was compared with that to distilled water alone. No significant effects of taste were found. In the second experiment five taste substances: HCl, fructose, NaCl, KCl and quinine were diluted with fluids normally imbibed by the embryo: amniotic and/or allantoic fluid taken from other eggs. These solutions and also distilled water were compared with egg-fluid alone. A highly significant effect of the five solutions was found showing that the taste system becomes functional before the time of hatching. Distilled water produced on an unexpectedly large response in the embryo; possible reasons for this are discussed.

Animals↗

Polarized distribution of the viral glycoproteins of vesicular stomatitis, fowl plague and Semliki Forest viruses in hippocampal neurons in culture: a light and electron microscopy study.

We have shown previously using immunofluorescence microscopy that upon infection of polarized hippocampal cells in culture with vesicular stomatitis virus (VSV) and fowl plague virus (FPV) the VSV glycoprotein is delivered to the plasma membrane of the dendrites and of the cell body whereas the FPV hemagglutinin is transported to the axonal surface (Cell, 62 (1990) 63-72). In this work electron microscopy of infected rat hippocampal neurons showed that VSV progeny budded from the plasma membrane of the dendrites and the cell body. The location of the budding virions corresponded to the distribution of the VSV glycoprotein which was detected over the somatodendritic plasma membrane by immunoelectron microscopy. In contrast, no FPV formation was seen in the infected neurons although the FPV hemagglutinin was localized to the axonal surface by immunoelectron microscopy. In Semliki Forest virus (SFV) infected hippocampal cells we observed that the viral glycoproteins were exclusively present in the dendrites and cell body but not in axons.

Animals↗

Quisqualate receptors in epileptic fowl: the absence of coupling between quisqualate and N-methyl-D-aspartate receptors.

The ability of excitatory amino acid receptor agonists, AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and quisqualate to produce seizures was determined in 1-2 day old epileptic and non-epileptic (carrier) chicks. Both compounds produced prolonged clonic seizures in epileptic chicks at doses which were not convulsant in carrier chicks. Seizures produced in epileptics by AMPA were suppressed by the quisqualate antagonist CNQX (6-cyano-7-nitroquinoxaline-2,3-dione), but were not prevented by pretreatment with competitive (2-amino-7-phosphonoheptanoic acid, APH) or non-competitive (MK-801) NMDA (N-methyl-D-aspartate) receptor antagonists. These data do not support the hypothesis that NMDA receptors work in concert with quisqualate receptors. Binding sites for [3H]AMPA were characterized in cerebral hemispheres of both epileptic and carrier chicks. Analysis of the data revealed no significant alterations in the binding affinity (KD) or the number of binding sites (Bmax) of AMPA to tissue preparations from epileptic chickens when compared to carriers. The latter data does not explain the increased susceptibility of epileptic fowl to the convulsant effects of quisqualate and AMPA.

Animals↗

Partial retinal dysplasia and subsequent degeneration in a mutant strain of domestic fowl (rdd).

An inherited recessive form of retinopathy has been discovered in the domestic fowl (rdd) which is characterized by progressive deterioration of the retina, culminating in blindness by sexual maturity. Morphologically, the condition is recognizable by abnormalities in both the retinal pigment epithelium and the neural retina. Gaps in the pigment epithelium which are first detected macroscopically at nine days of incubation become larger and more numerous until the time of hatching, then disappear during the subsequent week. Undulations in the outer nuclear, outer plexiform, and inner nuclear layers are obvious by 11 days of incubation. There is a marked reduction of photoreceptors at 18 days of incubation as compared to normal controls. After hatching, the thickness of the retina decreases with age, primarily due to cell loss from the photoreceptor region and inner nuclear layer. Detachment of the atrophic retinas generally occurs in adults, and is followed in some adults by granulation and ossification of the vitreous. Problems concerning the site of the lesion are discussed.

Aging↗

Histochemical demonstration of carbonic anhydrase and Na+/K+-ATPase in the pecten oculi of the fowl.

The distribution of carbonic anhydrase (CA) and Na+/K+-ATPase was studied histochemically in the pecten of the fowl by light and electron microscopy. No Na+/K+-ATPase activity was seen by the method used here. CA staining was seen in the membranes of the apical and basal microvilli of the endothelial cells, while the cytoplasm took no stain. There were no staining differences between the capillaries of the different regions of the pecten. Only the capillaries of the bridge showed no microvilli and no staining. Neither did arterioles and venules which lacked microvilli stain. The functional significance of the association of CA activity and microvilli is not clear.

Animals↗

Pharmacological studies on the noradrenergic control of luteinizing hormone secretion in the domestic fowl.

A neuropharmacological approach was utilized in order to investigate catecholaminergic involvement in the control of LH secretion in the domestic fowl. Inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine (alpha Mpt) at several doses was accompanied by significant reductions in the circulating LH concentration of 6-week-old male cockerels. Plasma LH was similarly depressed following the selective inhibition of NE synthesis by either diethyldithiocarbamate (DDC) or FLA 63. Blockade of alpha 1-adrenergic receptors with phenoxybenzamine was consistently associated with precipitous declines in plasma LH concentrations. Stimulation of alpha-adrenergic receptors by phenylephrine and clonidine elevated circulating LH levels. Activation of the dopaminergic system by apomorphine depressed LH release. However, pimozide was without effect. These data suggest that norepinephrine is involved in the stimulation of LH release, while dopamine may exert an inhibitory influence. Evidence of some stimulatory beta-adrenergic effect is also described.

Animals↗

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↗

Stimulatory and inhibitory effects of prostaglandin E2 on prolactin release in the domestic fowl.

In vivo prolactin secretion was increased in immature cockerels 20-30 min after the intravenous administration of prostaglandin (PG) E2 at a dose of 200 micrograms/kg. The addition of PGE2 to incubation medium had no direct effect on the release of pituitary prolactin during short-term (3-hr) culture, but augmented the stimulatory effect of hypothalamic tissue on prolactin secretion. The stimulatory effect of serotonin, noradrenaline, acetylcholine, and histamine on hypothalamus-induced prolactin release was also increased when pituitaries were coincubated with 10(-7)M PGE2, as was the stimulatory effect of thyrotrophin-releasing hormone (TRH) and hypothalamic extract (HE). The long-term (24-hr) preincubation of pituitaries with 10(-7)M PGE2 reduced the responsiveness of the prolactin-secreting cells to TRH or HE stimulation. PGE2 treatment also reduced the stimulatory effect of hypothalamic tissue on prolactin release and diminished the stimulatory effect of serotonin on hypothalamus-induced prolactin secretion. A 24-hr preincubation of hypothalamic tissue with 10(-7)M PGE2 also reduced its stimulatory effect on prolactin release when subsequently incubated with control pituitary glands. These results demonstrate that PGE2 initially stimulates in vivo and in vitro prolactin secretion in the fowl, possibly by increasing the release of hypothalamic prolactin-releasing activity and/or by increasing pituitary sensitivity to provocative stimuli. Chronic PGE2 stimulation appears to result in a reduction in pituitary responsiveness to stimulatory influences and in the release of hypothalamic-releasing activity.

Acetylcholine↗

Catecholamine involvement in the control of growth hormone secretion in the domestic fowl.

A neuropharmacologic approach was utilized to investigate the catecholaminergic influence on the hypothalamic regulation of growth hormone (GH) secretion in young (6-week-old) male domestic fowl. The selective inhibition of norepinephrine (NE) and epinephrine (E) synthesis or activity by diethyldithiocarbamate (DDC), FLA63 (dopamine-beta-hydroxylase inhibitors), phenoxybenzamine (alpha 1 receptor blocker), and yohimbine (alpha 1 and alpha 2 receptor antagonist) was associated with a decline in circulating GH levels. Similarly inhibition of NE reuptake by imipramine or desmethylimipramine were followed by reduced GH secretion. In the presence of alpha-methyl-p-tyrosine (alpha Mpt, a tyrosine hydroxylase inhibitor), the administration of phenylephrine (alpha 1 agonist) was followed by increased plasma concentrations of GH. However, alone, it was without effect. Similarly plasma concentrations of GH were elevated by dihydroxyphenylserine (DOPS, a precursor of NE/E) in chicks pretreated with DDC or carbidopa. These data are consistent with the stimulatory hypothalamic control of GH involving NE/E which exert their effects via alpha (probably alpha 1) postsynaptic stimulatory receptors. Evidence that it is E rather than NE, which is the catecholamine involved or the hypothalamic control of GH, comes from the decrease in plasma GH concentration following the inhibition of central E synthesis by SKF64139 (an inhibitor of phenylethanolamine-N-methyltransferase). Some evidence for a limited inhibitory dopaminergic system was found. Inhibition of dopamine (DA) synthesis by alpha Mpt produced significant elevations in plasma GH concentration. In addition, apomorphine (DA agonist) consistently depressed GH release. However, blockade of DA receptors by pimozide had either no effect on plasma GH concentrations or at a very high dose decreased plasma GH concentrations. NE/E also appear to have a depressive effect on plasma concentrations of GH in young chicks, probably via a peripheral site of action. Plasma concentrations of GH were reduced by the peripheral administration of NE, which might be expected not to cross the blood-brain-barrier (BBB), alpha 1/alpha 2 agonists clonidine and p-amino clonidine (which does not cross BBB), NE/E precursors L-DOPA and DOPS, and the beta agonist, isoproterenol. Furthermore, the depression of peripheral E synthesis (by SKF29661 which inhibits phenylethanolamine-N-methyltransferase) elevated the plasma concentration of GH.

Animals↗

Effect of Iodide, methimazole, and thyroxine on thyroidal accumulation of radioiodide in immature domestic fowl.

Accumulation of radioiodide by the thyroids of individual domestic fowl was measured with the technique described by T. F. Davison, J. G. Rowell, and J. Rea, [1981) J. Endocrinol. 89, 371-378). Radioiodide uptake was markedly decreased in birds given an excess of iodide in the drinking water (60 mg KI/liter) or injections of thyroxine (T4: 5 X 50 micrograms T4/kg body wt), in agreement with published findings. Treatment with a goitrogen (250 mg methimazole/liter drinking water) decreased 125I uptake for at least 8 days but thereafter uptake increased and this was accompanied by gross thyroidal enlargement. The results indicate that the thyroid partly compensates for goitrogenic inhibition.

Animals↗

Failure of castration to prevent the prepubescent decline in the circulating concentration of growth hormone in the domestic fowl.

In the domestic fowl, plasma concentrations of growth hormone (GH) have been observed to be elevated in young, rapidly growing chicks and low in older chicks and in adults. In this present study the plasma concentration of GH was high in 35-day-old male chickens and declined to the low adult concentration by 91 days of age. This decrease was observed in male chickens irrespective of whether they remained intact, were castrated at 35 days of age, or were castrated and implanted with testosterone. The plasma concentrations of GH in castrated birds were lower than those in the controls at 49 and 63 days of age. As would be expected, the plasma concentrations of luteinizing hormone (LH) were elevated by castration while testosterone implantation reduced the castration-induced rise in LH concentrations. Castration was followed by very low but detectable plasma concentrations of androgen. These were increased by testosterone implants.

Aging↗

Food intake regulation of circulating thyroid hormones in domestic fowl.

The relationship between food intake and thyroid function has been investigated in immature domestic fowl. Starvation delayed, but did not suppress, the triiodothyronine (T3) response to intravenously administered thyrotropin-releasing hormone (10 micrograms/kg). This probably resulted from a suppression of monodeiodinase activity, since the conversion of thyroxine (T4) to T3 in thyroidectomised birds following an intramuscular injection of T4 (10 micrograms/kg) was markedly reduced by starvation. Starvation, for 24 or 48 hr, lowered the circulating T3 level but increased the T4 concentration. When fasted birds were refed the T4 concentration was initially enhanced but subsequently declined as the T3 concentration progressively increased. The accompanying decline in the T4:T3 ratio in fasted-refed birds indicated that the rise in the T3 level resulted from the peripheral monodeiodination of T4. The increase in T3 concentration could be induced solely by carbohydrate; the intraperitoneal administration of glucose (2.0 g/kg) to fasted birds resulting in a slight, transient rise in the T3 concentration and a fall in the T4:T3 ratio. The generation of T3 was also energy dependent, in that the magnitude of the T3 response of fasted birds to refeeding was proportional to the amount of food consumed and to the metabolisable energy (ME) content of the diet. Moreover, when exogenous T4 (100 micrograms/kg) was intramuscularly administered to thyroidectomised birds fed a diet with a high ME content, the conversion of T4 to T4 was greater than that in birds fed a diet of lower ME content. These results demonstrate that nutritional stimuli are involved in the regulation of thyroid function in birds, particularly in the peripheral generation of T3.

Animals↗

The effect of exposure to 40 degrees on the heat production and the serum concentrations of triiodothyronine, thyroxine, and corticosterone in immature domestic fowl.

Four-week-old fowl were exposed to 40 degrees for 35 days and the effects on the serum concentrations of triiodothyronine (T3), thyroxine (T4), and corticosterone were investigated. Changes in resting heat production, food intake, body temperature, body weight gain, and growth (both in terms of skeletal growth and weight of selected organs) were also measured. Body temperature was increased at 40 degrees, and body weight gain and skeletal growth were both reduced. The serum concentrations of T3 and T4 were reduced at 40 degrees. The decrease in serum T3 was more strongly correlated with the reduction in food intake than was the reduction in T4. Resting heat production was decreased by exposure to 40 degrees; the reduction in heat production was correlated with serum T3 and serum T4 concentrations. Exposure to 40 degrees had no effect on adrenal weight or on serum corticosterone concentration but weights of the bursa, spleen, and thymus glands were decreased. These results suggest that (a) T3 is the principle metabolically active thyroid hormone in the chicken and that the reduction in heat production at 40 degrees is related to the decline in T3; (b) the reduction in T3 is a consequence of the reduction in food intake; and (c) the response to a stressor need not involve increased adrenocortical activity.

Animals↗

Growth hormone secretion in anaesthetized fowl. 1. Refractoriness to repeated stimulation by human pancreatic growth hormone-releasing factor (hpGRF) or thyrotrophin releasing hormone (TRH).

The intravenous (iv) administration of thyrotrophin releasing hormone (TRH, at 1.0 or 10.0 micrograms/kg) or human pancreatic growth hormone-releasing factor (hpGRF(1-44)NH2, at 10 micrograms/kg) markedly increased the growth hormone (GH) concentration in the plasma of immature or adult cockerels anaesthetized by sodium pentabarbitone (30 mg/kg, iv). A second injection of either TRH or hpGRF failed to increase the GH concentration in immature chicks when administered 15, 30, or 60 min after the first injection. However, significant GH responses to TRH or hpGRF were observed when the interval between injections was either 120 or 240 min. The magnitude of the GH responses to TRH were, however, diminished by 83.3 and 26.7% when given 120 or 240 min after the initial TRH injection, and the responses to hpGRF were similarly reduced by 68.3 and 33.6%. A similar period of GH refractoriness to TRH or hpGRF stimulation was also observed in adult birds, although the recovery of GH responsiveness occurred earlier. While a second injection of hpGRF was ineffective in increasing the plasma GH concentration if given within 30 min of the first, it was fully effective when the interval between injections was greater than 60 min. In response to a second injection of TRH, the GH concentration was elevated when the interval between injections was greater than 120 min, after which the magnitude of the response evoked was greater than that induced by the initial injection. Growth hormone secretion secretion in immature and adult fowl is therefore refractory to repeated provocative stimuli, although the mechanism involved is unknown.

Anesthesia↗

Growth hormone secretion in anaesthetized fowl. 2. Influence of heterologous stimuli in birds refractory to human pancreatic growth hormone-releasing (hpGRF) or thyrotrophin releasing hormone (TRH).

In anaesthetized young (6 weeks old) and adult (22-30 weeks old) domestic fowl, the administration of thyrotrophin releasing hormone (TRH; 1.0 micrograms/kg in young birds; 10.0 micrograms/kg in adults) or human pancreatic growth hormone-releasing factor (hpGRF(1-44)NH2; 10.0 micrograms/kg in both cases) markedly increased the growth hormone (GH) concentration in plasma samples collected 10 min later. In birds injected with TRH, this stimulation of GH secretion attenuated the GH response to a second TRH challenge (given 15 or 60 min after the first in adult or young birds, respectively); similarly, hpGRF pretreatment blunted the GH response to a further hpGRF injection. However, the administration of hpGRF to both immature and adult birds made refractory to TRH challenge was followed by increased GH secretion and vice versa. Moreover, the GH secretory response to hpGRF in birds pretreated with TRH was greater (1.99-fold in young birds, 1.52-fold in adults) than the increase in plasma GH concentration following hpGRF administration in untreated birds. Similarly, prior exposure to hpGRF also increased the GH response to TRH stimulation (by 2.24-fold in the young, 3.56-fold in the adults). These results demonstrate that TRH not only overcomes GH refractoriness to hpGRF and vice versa, but the GH response to heterologous provocative stimuli is potentiated in birds refractory to TRH or hp GRF challenge.

Anesthesia↗