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PubMed1975

[Morphogenesis of the chick embryo foot].

Observations were made on chick embryo feet between 6 and 12 1/2 days of incubation in order to (a) give a precise description of programmed cell death in the interdigital membranes; (b) correlate the evolution of interdigital necrosis with the differentiation of the cartilaginous phalangeal skeleton; (c) measure the relative growth rates of digits and interdigits. The programme of interdigital cell death proceeds in three phages which comprise the appearance, the extension and the disappearance of necrotic areas. Fourteen distinct stages are described. The evolution of programmed cell death can be strictly correlated to the chondrogenesis of successive phalanges, in the sense that each stage of necrosis (except two of them) differs from the preceding one by the differentiation of an additional phalanx. Shaping of the foot results from differential growth rates and proceeds in three phases, the second of which is characterized, between days 8 and 10 of incubation, by the actual shortening (decrease of absolute length) of the interdigital membranes. These observations are compared to those that were previously made on other avian and mammalian species and the morphogenetic role of programmed cell death is discussed in the light of that comparison.

Animals↗

PubMed1979

Morphology and behaviour of neural crest cells of chick embryo in vitro.

Neural primordia of chick embryos were cultured for three days and the behaviour of migrating neural crest cells studied. Somite cells were used as a comparison. Crest cells were actively multipolar with narrow projections which extended and retracted rapidly, contrasting to the gradual extension of somite-cell lamelleae. On losing cell contact, somite cells were also more directionally persistent. The rate of displacement of isolated crest cells was particularly low when calculated over a long time base. Both crest and somite cells were monolayered; contact paralysis occurred in somite cell collisions but was not ascertained for crest cells. However, crest cells in a population were far more directionally persistent than isolated cells. Contact duration between crest cells increased with time and they formed an open network. Eventually, retraction clumping occurred, initially and chiefly at the periphery of the crest outgrowth. Crest cells did not invade cultured embryonic mesenchymal or epithelial populations but endoderm underlapped them. No effects were observed on crest cells prior to direct contact. Substrate previously occupied by endoderm of ectoderm caused crest cells to flatten while substrate previously occupied by the neural tube caused them to round up and clump prematurely.

Animals↗

PubMed1999

Abnormal collagen assembly, though normal phenotype, in alginate bead cultures of chick embryo chondrocytes.

The collagens produced by chick embryo chondrocytes cultured in alginate beads were investigated both biochemically and ultrastructurally. The cartilage phenotype is maintained for at least 14 days, as indicated by the production of the cartilage-specific collagens II, IX, and XI and the absence of collagen I. There were differences in the distributions of collagens among the three different compartments analyzed (cells and their associated matrix, further-removed matrix (released by alginate solubilization), and culture medium), with large amounts of collagen IX (mainly in proteoglycan form) in the culture medium. Inhibition of lysyl oxidase activity by beta-aminopropionitrile led to an overall decrease in collagen production. In contrast to the biochemical observations, collagen ultrastructure in the extracellular matrix of alginate cultures was not in the form of the expected 64-nm banded fibrils, but rather in the form of segment-long-spacing-like crystallites. This abnormal structure is likely to be a result of alginate disrupting normal assembly. We conclude that, in this system, the native fibrillar structure of the collagenous matrix is not essential for the maintenance of the differentiated phenotype of chondrocytes.

Alginates↗

PubMed1990

The marginal zone and its contribution to the hypoblast and primitive streak of the chick embryo.

The marginal zone of the chick embryo has been shown to play an important role in the formation of the hypoblast and of the primitive streak. In this study, time-lapse filming, fate mapping, ablation and transplantation experiments were combined to study its contribution to these structures. It was found that the deep (endodermal) portion of the posterior marginal zone contributes to the hypoblast and to the junctional endoblast, while the epiblast portion of the same region contributes to the epiblast of the primitive streak and to the definitive (gut) endoderm derived from it. Within the deep part of the posterior marginal zone, a subpopulation of HNK-1-positive cells contributes to the hypoblast. Removal of the deep part of the marginal zone prevents regeneration of the hypoblast but not the formation of a primitive streak. Removal of both layers of the marginal zone leads to a primitive streak of abnormal morphology but mesendodermal cells nevertheless differentiate. These results show that the two main properties of the posterior marginal zone (contributing to the hypoblast and controlling the site of primitive streak formation) are separable, and reside in different germ layers. This conclusion does not support the idea that the influence of the posterior marginal zone on the development of axial structures is due to it being the source of secondary hypoblast cells.

Animals↗

PubMed1983

Effect of dexamethasone and combinations of hormones on 7-day chick embryo lung cells.

Seven-day chick embryo lung was dissociated into single cells and the capacity of these cells to incorporate 1-3H-glucosamine and 1-14C-glycine in a rotational-mediated aggregation system upon the addition of hormones was determined. Incorporation of 1-3H-glucosamine was stimulated 50% by 10(-8) M dexamethasone while 1-14C glycine uptake was not markedly influenced. Dexamethasone, 10(-8) M and 10(-6) M insulin gave rise to a 90% enhancement in 1-3H-glucosamine incorporation and a 20% increase in 14C-glycine uptake. When the aggregating cells were incubated with 10(-8) M dexamethasone and 10(-8) M 3,3',5-tri-iodo-thyronine, glucosamine incorporation was augmented by 40% and glycine by 25%. The combination, 10(-8) M 3,3',5-tri-iodo-thyronine, 10(-8) M dexamethasone and 10(-6) M insulin led to a 70% stimulation in glucosamine labelling and a 50% increase in 1-14C-glycine uptake. Very little change in the incorporation of the hexosamine and glycine into the soluble culture media was observed by adding either of the hormones; however, there appeared to be a slight increase in the incorporation of both tracers when the cells were incubated with the combination of dexamethasone and insulin.

Animals↗

PubMed1989

Regulation of production of delta-aminolaevulinate synthase in tissues of chick embryos. Effects of porphyrogenic agents and of haem precursors.

Studies conducted by several groups have established that porphyrogenic agents which caused elevations in chick-embryo liver delta-aminolaevulinate (ALA) synthase activity also increased the concentrations of the enzyme's RNA, and that haemin inhibited these elevations. We have determined in this study, using immune-blot analyses, that administration in ovo of allylisopropylacetamide (AIA) in combination with diethyl 1,4-dihydro-2,4,6-trimethyl,3,5-pyridinedicarboxylate (DDC) increased the mass of ALA synthase in intestine and kidney of chick embryos. Furthermore, the molecular mass of the subunit of the enzyme in those tissues appeared identical with that of liver ALA synthase. Using a synthetic oligonucleotide complementary to ALA synthase mRNA, we determined by solution hybridization and Northern-blot analyses that AIA and DDC also increased the concentrations of ALA synthase mRNA in intestine and kidney and that testosterone elevated the concentration of the RNA in kidney. In analyses of RNA obtained from chick-embryo liver, intestine, kidney, heart, brain and lung, the probe bound primarily in each case to a single 2.3 kb RNA. Finally, the haem precursors ALA and FeCl3, when injected together into the fluid surrounding embryos, inhibited both the elevations in ALA synthase mass and RNA concentration brought about by porphyrogenic agents in liver, kidney and intestine. Thus the results indicated that: (1) certain porphyrogenic agents increased ALA synthase mass and RNA in chick-embryo intestine and kidney, in addition to liver; (2) ALA and FeCl3 inhibited the elevations; and (3) the sizes of ALA synthase's subunit as well as the enzyme's mRNA appeared identical, in each case, in all tissues examined.

5-Aminolevulinate Synthetase↗

PubMed1979

Observations on closure of the neuropores in the chick embryo.

Neuropore closure was studied in chick embryos by light and electron microscopy. Surface ectoderm reflects over the crests of the neural folds at all craniocaudal levels, merging with the neural ectoderm lining the neural groove. Apices of surface ectodermal cells have an essentially identical morphology prior to approximation of folds, both within the presumptive fusion sites and more laterally. Cells of these areas have slightly convex profiles exhibiting few cellular protrusions. Each neural fold contains a superficial half, composed of neural ectoderm covered by surface ectoderm, and a deep half consisting entirely of neural ectoderm. Initial contact between folds usually occurs near the junction between these halves in cranial regions, but is restricted primarily to surface ectoderm at caudal levels. Subsequent fusion of folds at all levels involves both ectodermal layers. Cellular protrusions and small, morphologically unspecialized intercellular junctions often interconnect cells of apposed folds in areas undergoing fusion. The anterior neuropore closes at stages 10-11, but fusion of folds in this region is not completed until stages 13-14. Fusion occurs dorsoventrally in this area and is more advanced internally than externally. Numerous pleomorphic inclusions and a few apparently necrotic cells are present in areas bordering the anterior neuropore. The posterior neuropore closes at stages 12-13 and fusion is completed in this region during stages 13-14. The caudal end of the posterior neuropore closes dorsal to the developing tail bud. Several morphological features of this closure may at least partially account for the high susceptibility to myeloschisis localized specifically at caudal spinal cord levels.

Animals↗

PubMed1983

Transformation by Rous sarcoma virus induces similar patterns of glycosaminoglycan synthesis in chick embryo skin fibroblasts and vertebral chondroblasts.

Chick embryo skin fibroblasts and vertebral chondroblasts were infected with a temperature-sensitive mutant of Rous sarcoma virus, LA24A, and were grown at permissive (36 degrees C) and nonpermissive (41 degrees C) temperatures. During exponential growth, infected and parallel uninfected cultures were labeled with D-[3H]glucosamine, and newly synthesized glycosaminoglycans were identified by anion exchange chromatography and by selective enzymatic and chemical degradations. Control fibroblasts synthesized low levels of hyaluronic acid (HA), and dermatan sulfate (DS), moderate levels of heparan sulfate (HS), and high levels of chondroitin sulfate (CS). In contrast, control chondroblasts synthesized very low levels of HA and DS, no HS, and very high levels of CS. Following transformation and growth at 36 degrees C, both cell types showed a dramatic increase in HA synthesis and a significant decrease in CS synthesis. In addition, transformed chondroblasts initiated the synthesis of HS and increased their synthesis of DS to levels that matched those of transformed fibroblasts. The CS chains synthesized by control chondroblasts were partially undersulfated, while those synthesized by both normal and transformed fibroblasts were fully sulfated. Upon transformation, chondroblasts grown at 36 degrees C initiated the synthesis of fully sulfated CS chains. Most of the above biosynthetic alterations were completely reversed when infected cells were grown at 41 degrees C, indicating that they were dependent on the transforming gene product of LA24A. Clearly, the profound differences that distinguish normal fibroblasts from normal chondroblasts are lost upon transformation, and these two types of terminally differentiated cells converge toward a common, though not identical, biosynthetic program for glycosaminoglycans.

Animals↗

PubMed1997

Stimulation of 5-HT1A receptor inhibits apoptosis induced by serum deprivation in cultured neurons from chick embryo.

Primary cultures of neurons from chick embryo telencephalons were deprived of serum to induce apoptotic cell death. After 24 h of serum withdrawal, we found a reduction in cell viability from 85% to 72% and an increase in the number of apoptotic cells from 12% to 29%. The 5-HT1A receptor agonist 8-OH-DPAT inhibited the decrease in cell viability and reduced the number of apoptotic cells in a concentration-dependent manner. The anti-apoptotic effect of 8-OH-DPAT (1 microM) could be blocked by adding the selective 5-HT1A antagonist MPPI (10 microM), but not in the presence of the dopamine receptor antagonist chlorpromazine (1 microM) and of the beta-receptor blocker propranolol (10 microM). In addition, anti-nerve growth factor (NGF) antibodies inhibited the protective effect of 8-OH-DPAT, suggesting that induction of NGF was involved in the mechanism of action. Serum deprivation alone already induced a release of NGF (10 pg/flask) which protected the neurons from further cell death. Accordingly, the addition of the same amount of exogenous NGF restored cell viability up to control level and addition of anti-NGF antibodies further decreased cell viability to 56%. In the presence of 8-OH-DPAT (1 microM), the level of NGF in the culture medium was only slightly yet consistently increased compared to serum deprivation from 4 h onwards. Thus, our data suggest that the anti-apoptotic effect of 8-OH-DPAT is mediated by the stimulation of 5-HT1A receptors. Furthermore, the induction of neuronal NGF synthesis and secretion contributes to its neuroprotective action.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2001

Apoptosis and necrosis occurring in excitotoxic cell death in isolated chick embryo retina.

Excitotoxic studies using isolated chick embryo retina indicated that such an in vitro model provides a valid tool to characterize the effect of different agonists for subtypes of glutamate ionotropic receptors. In retinas maintained for 24 h in a Krebs medium, after a brief exposure (30 min) to glutamate agonists, we compared the effects produced by NMDA and non-NMDA-agonists, such as kainic acid (KA) or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). Delayed retinal damage was assessed by measuring lactate dehydrogenase (LDH) present in the medium after exposure to the previously named agonists. Although at high concentrations, both KA and AMPA produced more relevant release than NMDA, 7-8% of total retinal LDH was released after exposure to a 50 microM concentration of non-NMDA agonists. These values were similar to those obtained after 100 microM NMDA. In this regard, retinal tissue appeared to be less sensitive to excitotoxicity based on the activation of NMDA receptor subtype. All three agents produced histopathological lesions typical for excitotoxic damage. A delayed form of excitotoxicity observed in retina segments was predominated by necrotic features. However, the activation of apoptotic machinery early during the incubation period subsequent to brief exposure to NMDA (100 microM) was also present. The activation of caspase enzymes was studied by a fluorometric protease activity assay as well as by western blot analysis. Caspase-3-like activity reached the highest value within 3 h of incubation after exposure to excitotoxin, then the level of enzyme activity declined to lower values. As confirmed by a time-related appearance of TUNEL-positive nuclei, apoptotic features appeared to be specific for retina response to NMDA. In contrast, the exposure to a 50 microM concentration of KA or AMPA induced necrotic cell damage which was evident through the incubation, leading to a delayed mechanism of excitotoxicity. These observations provide evidence that in the retinal model, with regard to agonist concentrations and subtype of glutamate receptors, the cascade of events leading to excitotoxicity may result in either apoptotic or necrotic neuronal cell damage.

Animals↗

PubMed1982

Acetylcholinesterase in neural tube defects: a model using chick embryo amniotic fluid.

Acetylcholinesterase was measured in amniotic fluid from normal chick embryos and embryos with neural tube defects. Neural tube defects were induced in the chick embryos by three procedures, removal of albumen, mechanical disruption of the closed neural tube or injection of tetanus toxin. The concentration of acetylcholinesterase in amniotic fluid from untreated normal embryos changed throughout the period examined (5-14 days incubation) but was stable at 0.5 U1(-1) over the time period 6-11 days. Amniotic fluid taken from treated embryos with neural tube defects at 8 days always contained a higher concentration of acetylcholinesterase than fluid from sham operated but otherwise normal embryos, mean 40.9 U1(-1), S.E.M. = 10. U1(-1), versus 1.0 U1(-1), S.E.M. = 0.2 U1(-1). The range of values (6.1-393 U1(-1)) was clearly separated from the normal values, range 0.0-5.5 U1(-1). In 13 cases with developmental abnormalities other than neural tube defects, the concentration of acetylcholinesterase was elevated in only one. Two different forms of acetylcholinesterase, as shown by gel electrophoresis, were present in fluid form both normal and defective embryos. These forms were also present in blood plasma, cerebrospinal fluid and in the high speed supernatant from brain extracts, the latter tissue contained an additional form of greater electrophoretic mobility. After irreversible inhibition, enzyme activity in amniotic fluid recovered slowly; only half the control value was reached by 140 h compared with complete recovery in the tissues of the embryo within 19 h. Histochemical staining for acetylcholinesterase showed that the spinal cord in the region of the lesion contained high concentrations of the enzyme. The possible sources of acetylcholinesterase in amniotic fluid are discussed. This chicken model of neural tube defects provides support for the use of acetylcholinesterase tests in the detection of neural tube defects clinically, and provides a model for experimentation with this system.

Acetylcholinesterase↗

PubMed1989

Histochemical studies of the vestibular nerve system in the developing chick embryo. Glycoconjugates in the vestibular end organs.

Glycoconjugates of the vestibular end organs in the developing chick embryos were well defined and localized using lectins-HRP (WGA, PNA, UEA-1) and HID-AB stains. In spite of the fact that no differentiation of the otic vesicle was seen on the 4-day-old chick embryos, the luminal surface of the otic vesicle was labeled with lectins. The cupula and otoconia were labeled most intensely with lectins on the 6-day-old chick embryos. The reactivity of lectins with the cupula and otoconia was as follows: WGA greater than UEA-1 greater than PNA. As the vestibular end organs had become mature, the epithelial cells of the semicircular duct, utricle and saccule were labeled with lectins. These findings suggest that glycoconjugates play an important role in the development and formation of the vestibular end organs.

Animals↗

PubMed1997

The effect of pulsed and sinusoidal magnetic fields on the morphology of developing chick embryos.

Several investigators have reported robust, statistically significant results that indicate that weak (approximately 1 microT) magnetic fields (MFs) increase the rate of morphological abnormalities in chick embryos. However, other investigators have reported that weak MFs do not appear to affect embryo morphology at all. We present the results of experiments conducted over five years in five distinct campaigns spanning several months each. In four of the campaigns, exposure was to a pulsed magnetic field (PMF); and in the final campaign, exposure was to a 60 Hz sinusoidal magnetic field (MF). A total of over 2500 White Leghorn chick embryos were examined. When the results of the campaigns were analyzed separately, a range of responses was observed. Four campaigns (three PMF campaigns and one 60 Hz campaign) exhibited statistically significant increases (P > or = 0.01), ranging from 2-fold to 7-fold, in the abnormality rate in MF-exposed embryos. In the remaining PMF campaign, there was only a slight (roughly 50%), statistically insignificant (P = 0.2) increase in the abnormality rate due to MF exposure. When the morphological abnormality rate of all of the PMF-exposed embryos was compared to that of all of the corresponding control embryos, a statistically significant (P > or = .001) result was obtained, indicating that PMF exposure approximately doubled the abnormality rate. Like-wise, when the abnormality rate of the sinusoid-exposed embryos was compared to the corresponding control embryos, the abnormality rate was increased (approximately tripled). This robust result indicates that weak EMFs can induce morphological abnormalities in developing chick embryos. We have attempted to analyze some of the confounding factors that may have contributed to the lack of response in one of the campaigns. The genetic composition of the breeding stock was altered by the breeder before the start of the nonresponding campaign. We hypothesize that the genetic composition of the breeding stock determines the susceptibility of any given flock to EMF-induced abnormalities and therefore could represent a confounding factor in studies of EMF-induced bioeffects in chick embryos.

Abnormalities, Radiation-Induced↗

PubMed1979

Lipid and carbohydrate metabolism in euthyroid and hypothyroid chick embryo (Gallus domesticus).

1. The effect of propylthiouracil (PTU)-induced hypothyroidism on carbohydrate and lipid metabolism was studied in the chick embryo. 2. A single dose of PTU (250 micrograms/embryo) was administered on day 11 and embryos sacrificed on day 20 of incubation. 3. Thyroid glands were significantly enlarged (6 fold) by PTU administration. 4. Increased thyroid weight was associated with growth retardation and decreased plasma thyroxine levels. 5. Plasma glucose level was lower and phospholipids were significantly higher in the hypothyroid embryo. 6. Liver lipid concentrations in the control and hypothyroid embryos were not different but were significantly higher in both groups when compared to previously reported values in the young chick. 7. In contrast to PTU treatment after hatching, liver glycogen levels were not increased in the hypothyroid chick embryo. This was attributed to the high lipid nutrient condition of the chick embryo since a high lipid diet in the young chick decreased hepatic glycogen accumulation significantly.

Animals↗

PubMedDate not supplied

[Compatibility of chick embryo eye anlagen with the ectoderm of the early amphibian gastrula in vitro].

Eye vesicles were isolated from the early chick embryos (stage 9+ after Hamburger and Hamilton, 1951) and combined with the Rana temporaria early gastrula ectoderm (EGE) in vitro. The tissues were jointly incubated in medium 199 diluted twice with deionized water at 22 +/- 1 degree for 7-8 days or the eye vesicles were removed from the EGE ectoderm within 16-18 h. At the joint long-term incubation of these tissues, a toxic effect of the chick embryonic tissues on the EGE cells was noted. In none of the experiments, the inducing effect of the eye vesicle on the EGE was found. Similar data were obtained when the EGE was jointly cultivated with the brain (stage 9-10) and retina (stage 15) of chick embryos. The brain of the chick embryos at stage 15 exerted a weak neuralizing effect on the EGE. In the control experiments, the eye vesicles explanted with the chick embryonic ectoderm remained viable till the end of cultivation but no lentoids formed in the ectoderm. The absence of lens-inducing effect at the joint cultivation of the chick embryonic eye vesicles with the EGE is considered as a result of disturbance of the synthesis or secretion of the corresponding agents rather than a sequence of the species "incompatibility" of the inductor and reacting tissue. Hence, the use of "xenogenic" tissue recombinants is not justified when analyzing the lens-inducing activity of the eye vesicles.

Animals↗

PubMed1987

17 Beta-estradiol secretion by the ovary of the hypophysectomized chick embryo.

Ovaries of intact and hypophysectomized 16-day-old chick embryos were cultured in medium 199 for 24 hr, and 17 beta-estradiol released into the culture media was measured by radioimmunoassay. The difference of the means of the two series of measurements was not significant. It is concluded that 17 beta-estradiol secretion by the chick embryo ovary is not under pituitary control, at least not before the stage of 16 days of incubation.

Animals↗

PubMed1982

Changes in sterol metabolism in the skin of developing chick embryo and alterations in the presence of an anticholesterolemic agent and a chemical carcinogen.

Changes in sterol metabolism in the skin of chick embryo during its development were studied with embryonal chick skin and with the cultured skin tissues. Changes in sterol metabolism of the skin of chick embryo began to appear at day 17, as observed by the accumulation of dihydrolanosterol, and the ratio of dihydrolanostrol:cholesterol increased thereafter until hatching. A similar change in sterol metabolism was also observed with the cultured skin tissue of chick embryo, although the stages of development seem to have been delayed by 3 days. The active sterol metabolism of the cultured skin tissue was also confirmed by studies of incorporation of [2-14C]acetate into sterols. 20,25-Diazacholesterol almost completely inhibited the incorporation of [2-14C]acetate into C27 sterols, whereas a chemical carcinogen, 4-hydroxyaminoquinoline 1-oxide, inhibited the incorporation of [2-14C]acetate into lathosterol but not that into cholesterol.

4-Hydroxyaminoquinoline-1-oxide↗

PubMed1990

Effect of ethanol on brain biogenic amines and phospholipids in the chick embryo.

The role of biogenic amines and phospholipids in the acute and chronic effects of ethanol on chick embryo development were studied. Injection of ethanol into chicken eggs on the third day of embryonic development produced no deficits in body or brain weight in the 17-day-old embryo. Spontaneous fetal motility of the 17-day old embryo did not differ between vehicle- and ethanol-treated groups, but acute administration of ethanol decreased motility. Ethanol decreased dopamine and homovanillic acid, while the level of serotonin and 5-hydroxyindoleacetic acid did not change in the 17-day-old chick embryo brain. Furthermore, lysophosphatidylcholine, phosphatidylcholine and phosphatidyl-ethanolamine turnover was decreased by ethanol. Ethanol decreased embryo viability in a dose-dependent manner as early as day 7. At this time, radiolabeled ethanol could be detected in the embryo. Thereafter, the levels of radiolabeled ethanol in whole embryos or embryo brains revealed continual exposure to ethanol throughout development. Our data suggest that monoaminergic neurons are involved in the development of ethanol tolerance through phospholipid synthesis in the chick embryo brain.

Animals↗