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Biomedical subjects

A A Moscona

Publications and source records attributed to A A Moscona.

At least 55 records · Page 3Linked to original sources
PubMed1981

Carbonic anhydrase C in the neural retina: transition from generalized to glia-specific cell localization during embryonic development.

The developmental profile and cellular localization of carbonic anhydrase C (carbonate dehydratase; carbonate hydro-lyase, EC 4.2.1.1) in the neural retina of chicken embryos and adults were investigated by immunochemical and immunohistochemical methods. Carbonic anhydrase C is present in the retina by the 3rd day of embryonic development. In the undifferentiated retina, it is detectable in virtually all the cells; however, as cell specialization progresses, its level declines rapidly in the emerging neurons and increases in Müller glia cells. An exception is certain amacrine neurons that contain carbonic anhydrase C to about the 16th day of development. In the adult retina, the enzyme is confined exclusively to Müller cells (the only gliocytes in the retina). Their identification was confirmed by immunostaining for glutamine synthase, an established Müller cell "marker." The presence in the mature retina of both these enzymes in Müller cells indicates that retinal gliocytes combine functional features that, in the brain, are segregated in astrocytes and oligodendrocytes. In the embryonic retina, carbonic anhydrase C and glutamine synthase differ markedly in their developmental profiles, cellular distribution, and susceptibility to regulation by cortisol and by cell interactions. Such differences make these two enzymes an attractive "marker team" for studying developmental mechanisms in embryonic retina and specific functions of Müller cells.

Animals↗
PubMed1981

Normal development and precocious induction of glutamine synthetase in the neural retina of the quail embryo.

The developmental pattern of glutamine synthetase (GS) in the neural retina of the quail embryo is described and correlated with retina growth and differentiation. We show that GS in the quail retina can be precociously induced by cortisol, and that the enzyme is localized in Müller glia cells. The results are compared with the development and induction of GS in chick retina.

Animals↗
PubMed1981

Developmental changes in the distribution of S-100 in avian neural retina.

Localization of S-100 in cells of embryonic and mature chick neural retina was studied by immunostaining of tissue sections with antiserum to S-100 and indirect immunofluorescence. Immunostaining was found to be localized predominantly in the neurons. In embryonic retina, the intensity of immunostaining increased transiently in each class of neurons at the time when they were undergoing organization within their stratum. Late embryonic and mature retina reacted weakly with the antiserum, with the exception of certain 'giant' ganglion cells that immunostained intensely. Müller cells, the only kind of glia cells in the chicken transiently in each class of neurons at the time when they were undergoing organization within their stratum. Late embryonic and mature retina reacted weakly with the antiserum, with the exception of certain 'giant' ganglion cells that immunostained intensely. Müller cells, the only kind of glia cells in the chicken transiently in each class of neurons at the time when they were undergoing organization within their stratum. Late embryonic and mature retina reacted weakly with the antiserum, with the exception of certain 'giant' ganglion cells that immunostained intensely. Müller cells, the only kind of glia cells in the chicken retina, did not react prominently with the antiserum at any of the stages examined and could not be discerned by immunostaining either in embryonic or in mature retina. The results indicate that in chick neural retina S-100 is found predominantly in neurons, and it increases and declines in different subpopulations of neurons coordinately with changes in the development and maturation if this tissue.

Animals↗
PubMed1980

Age-dependent differences in cognin regeneration on embryonic retina cells: immunolabeling and SEM studies.

The retina cognin (a glycoprotein isolated from the surface membrane of neural retina cells of chick embryos and postulated to mediate self-recognition and histogenetic association of retina cells) has been visualized by SEM on the surface of embryonic retina cells in vitro following immunolabeling of the cells with antibodies to the purified cognin and with polystyrene latex microbeads. Trypsin dissociation of retina tissue into separated cells resulted in cognin depletion from the cell surface; following incubation at 37 degrees C the cells regenerated the cognin. Regeneration was fastest and most abundant on cells from the youngest retinas examined; it declined markedly with the embryonic age of the cells, suggesting an age-dependent decrease in cell capacity for cognin formation. Evidence is discussed that the rate and amount of cognin regeneration on the cell surface are temporally-causally correlated with the capacity of the cells to reaggregate into retinotypic tissue. The results support the suggested role of the cognin in the mechanism of self-affinity and morphogenetic association of embryonic neural retinal cells.

Animals↗
PubMed1979

Induction of glutamine synthetase in embryonic neural retina: localization in Müller fibers and dependence on cell interactions.

The cellular localization of glutamine synthetase [GSase; L-glutamate:ammonia ligase(ADP)-forming), EC 6.3.1.2] induced by cortisol in the neural retina of chicken embryos was investigated by immunostaining with GSase-specific antiserum and indirect immunofluorescence. In organ cultures of retina tissue, and in the retina in vivo, hormone-induced GSase was found to be confined only to the Müller fibers (retinoglia). Also, in mature chicken retina, which contains a very high level of GSase, the enzyme was detected solely in Müller fibers. In short-term monolayer cultures of dispersed embryonic retina cells, there was no GSase induction and no immunodetectable increase in enzyme level. However, when the dispersed cells were reaggregated and they restituted retinotypic cell associations, GSase could be induced and it was localized in Müller fibers. The results suggest that, in addition to the hormonal stimulus, contact-dependent interactions between Müller glia cells and retina neurons are involved in the mechanism of GSase induction in the retina.

Animals↗
PubMed1979

The development of inducibility for glutamine synthetase in embryonic neural retina: inhibition by BrdU.

The hydrocortisone-mediated induction of glutamine synthetase (GS) in the neural retina of the chick embryo is a characteristic and unique feature of differentiation of this tissue. The induction involves genomic activity elicited by the inducer resulting in synthesis and accumulation of the enzyme. We describe correlations between the growth of embryonic retina tissue in vivo and in vitro and the development of its inducibility for GS, and demonstrate that this development proceeds through two phases: competence-acquisition phase (before the 7th day of development), and maturation phase. BrdU applied for 24 h to retinas of 5-day embryos irreversibly suppresses the development of induction-competence. However, BrdU does not affect the progressive maturation of inducibility when applied to retinas that already are fully induction-competent (8 days and older). The short treatment with BrdU of 5-day retinas also causes defective histogenesis resulting in drastic malformation of the tissue. The nature of the processes involved in competence-acquisition and in the maturation of inducibility for GS are examined. Possible mechanisms by which BrdU prevents the development of induction-competence for GS in the early embryonic retina and elicits defective histogenesis are discussed.

Animals↗
PubMed1979

Malformation of embryonic neural retina elicited by BrdU.

Exposure of neural retina tissue from early chick embryos (5 and 6-days) to 5-bromo-2'-deoxyuridine (BrdU) for 24 h irreversibly prevented normal histogenesis and resulted in the formation of chaotically disorganized tissue. The sensitivity of the retina to this effect decreased with embryonic age and declined sharply after the commencement of cell stratification. Examination by electron microscopy revealed the following progressive morphologic changes resulting from BrdU treatment: complete breakdown of the outer limiting membrane due to disappearance of its constituent tight junctions which normally anchor cells at the outer retinal surface; collapse and endocytosis of cilia, resulting in the absence of photoreceptor processes; increasing disorganization of the cells which commenced at the outer surface of the retina and progressed inward, resulting in chaotic distortion of the histologic architecture of the retina. Ultrastructural differences were noted between cells in the malformed retina, indicating the presence of several cell types. Possible mechanisms of this BrdU-elicited malformation are considered in the Discussion.

Bromodeoxyuridine↗
PubMed1977

Glutamine synthetase induction in embryonic neural retina. Interactions of receptor-hydrocortisone complexes with cell nuclei.

In the neural retina of the chick embryo, hydrocortisone (HC) elicits differential gene expression resulting in the induction of glutamine synthetase (GS), which is an enzyme marker of differentiation in the retina. The relationship between nuclear binding of receptor-hydrocortisone (R-HC) complexes and GS induction was investigated in cultures of retina tissue from 12-day chick embryos. The number of HC binding sites in the cytoplasm was estimated as 1650+/-200 per retina cell; there are approximately 1500+/-100 acceptor sites for R-HC per retina nucleus. GS induction in the retina became detectable only after R-HC bound to more than 40% of the nuclear acceptors sites; increased binding coincided with higher induction levels, until complete site saturation was attained; Proflavine, which blocks preferentially and completely GS induction in the retina by interfering in the nucleus with the enzyme-inducing action of the hormone, reduced nuclear binding of R-HC by only 20%; thus, only part of the R-HC that binds in the nucleus appears to be directly involved in eliciting the induction of GS. Within one hour after exposure of the retina to an inducing dose of HC, there was translocation of HC and HC-receptors (as R-HC complexes) from the cytoplasm into the nucleus and saturation of nuclear accepegan to decline; in 12 h, it was reduced to 50% of the initial saturation level. Since, during this time, the enzyme activity to increase, persistence of the induced state depends on association of the hormone with only a portion of the sites in the nucleus to which it can bind. The decrease in the amount of bound HC in the nuclei of induced cells was accompanied by an increase in the level of HC receptors in the cytoplasm. About 50% of this increase could be prevented by cycloheximide; this suggests that the reappearance of HC receptors in the cell cytoplasm may be due, at least in part, to de novo synthesis of HC receptors.

Animals↗
PubMed1977

Effects of cytosine arabinoside on differential gene expression in embryonic neural retina. II. Immunochemical studies on the accumulation of glutamine synthetase.

Cytosine arabinoside (Ara-C) elicits a significant increase in the level of the enzyme glutamine synthetase (GS) while it markedly reduces overall RNA and protein synthesis in cultures of embryonic chick neural retina. This increase was analyzed by radioimmunochemical procedures and compared with the induction of GS by hydrocortisone (HC). Accumulation of GS in Ara-C-treated retinas was found to be due to de novo synthesis of the enzyme; however, unlike the induction of GS by HC, Ara-C caused no measurable increase in the rate of GS synthesis. The results indicate that Ara-C facilitates GS accumulation largely by preventing degradation of the enzyme. Even though Ara-C inhibits the bulk of RNA synthesis in the retina, it does not stop the formation of GS-specific RNA templates. However, the progressive accumulation of these templates does not result in an increased rate of GS synthesis unless Ara-C is withdrawn from such cultures under suitable experimental conditions. Thus, it is suggested that the continuous presence of Ara-C imposes a reversible hindrance at the translational level which limits the rate of GS synthesis. The results demonstrate that the increase in retinal GS elicited by Ara-C is achieved through mechanisms which are quite different from those involved in the hydrocortisone-mediated induction of this enzyme.

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