Search PubMed⌕ Search

Biomedical subjects

G Levi

Publications and source records attributed to G Levi.

At least 145 records · Page 8Linked to original sources
PubMed1991

The distribution of E-cadherin during Xenopus laevis development.

A vast amount of experimental evidence suggests that cell surface molecules involved in cell-to-cell and/or cell-to-substrate interactions participate in the control of basic events in morphogenesis. E-cadherin is a cell adhesion molecule directly implicated in the control of Ca2(+)-dependent interactions between epithelial cells. We report here the patterns of expression of E-cadherin in developmental stages of Xenopus laevis ranging from early embryo to adult using immunofluorescence microscopy. Although its distribution shares some similarities with those of L-CAM in the chicken and E-cadherin/Uvomorulin in the mouse, the distribution of E-cadherin in Xenopus presents several peculiar and unique features. In early stages of Xenopus development, E-cadherin is not expressed. The molecule is first detectable in the ectoderm of late gastrulas (stage 13-13.5 NF). At this time both the external and the sensory layer of the nonneural ectoderm accumulate high levels of E-cadherin while the ectoderm overlying the neural plate and regions of the involuting marginal zone (IMZ) not yet internalized by the movements of gastrulation are E-cadherin-negative. Unlike most other species, endodermal cells express no or very low levels of E-cadherin up to stage 20 NF. Endodermal cells become strongly E-cadherin-positive only when a well-differentiated epithelium forms in the gut. No mesodermal structures are stained during early development. In the placodes, in contrast to other species, E-cadherin disappears very rapidly after placode thickening. During further embryonic development E-cadherin is present in the skin, the gut epithelium, the pancreas, many monostratified epithelia and most glands. Hepatocytes are stained weakly while most other tissues, including the pronephros, are negative. In the mesonephros, the Wolffian duct and some tubules are positive. During metamorphosis a profound restructuring of the body plan takes place under the control of thyroid hormones, which involves the degeneration and subsequent regeneration of several tissues such as the skin and the gut. All newly formed epithelia express high levels of E-cadherin. Surprisingly, degenerating epithelia of both skin and intestine maintain high levels of the protein even after starting to become disorganized and to degenerate. In the adult, staining is strong in the skin, the glands, the lungs, the gut epithelium and the pancreas, weak in the liver and absent from most other tissues. Our results show that the expression of E-cadherin in Xenopus is strongly correlated with the appearance of differentiated epithelia.

Animals↗
PubMed1991

EP-cadherin in muscles and epithelia of Xenopus laevis embryos.

EP-cadherin is a novel Xenopus Ca+2-dependent adhesion molecule, which shares comparable homology with mouse E- and P-cadherins (Ginsberg, De Simone and Geiger; 1991, Development 111, 315-325). We report here the patterns of expression of this molecule in Xenopus laevis embryos at different developmental stages ranging from cleavage to postmetamorphic. EP-cadherin is already expressed in the oocyte and egg and can then be detected in close association with the membrane of all blastomeres up to late blastula stages. Starting at late gastrula stages, the level of EP-cadherin expression increases sharply in non-neural ectodermal cells, in the somites and in the notochord; it persists in endodermal cells and decreases rapidly in all migratory cells. During neurulation the level of EP-cadherin expression declines gradually in the nervous system and is undetectable here throughout later development except in the optic nerve and in the neural part of the olfactory organ. This pattern continues during later development so that in the tailbud stage and up to metamorphosis the most prominent staining is detected in the epidermis and skeletal muscle. After metamorphosis, the molecule gradually disappears from the muscle tissue and the major site of expression remains the skin. EP-cadherin is invariably present in close association with the cell membrane. In the muscle it is associated with the sarcolemma at regions of myoblast-myoblast or myotube-myotube contact. In epidermal cells, EP-cadherin is usually coexpressed with E-cadherin. Yet, while E-cadherin staining is always restricted to the basolateral aspects of the cells, EP-cadherin is often distributed throughout the plasmalemma including the apical surface.

Animals↗
PubMed1991

Muscle differentiation in Xenopus laevis is characterized by particular states of vinculin phosphorylation.

Vinculin is a 130 kD cytoskeletal protein which is involved in the anchorage of actin microfilaments to the plasma membranes at sites of cell-cell and cell-matrix contacts. In this paper we prove that smooth and cardiac muscles of Xenopus laevis contain a specific isoform of vinculin not present in any other tissue including skeletal muscle and epithelia and we demonstrate that this form of the molecule is characterized by a specific state of phosphorylation. These data are discussed in view of the importance of posttranslational modifications of structural proteins, such as vinculin, in the determination of cellular behaviour during differentiation and development.

Animals↗
PubMed1990

Establishment of a permanent rat brain-derived glial cell line as a source of purified oligodendrocyte-type 2 astrocyte lineage cell populations.

A permanent glial cell line (L3) has been established from mixed glial cultures obtained from neonatal rat forebrain by repetitive passaging and selection of the process-bearing cells growing on top of a flat cell monolayer. Continuous propagation of the process-bearing cells was supported by the flat cells, of presumed astroglial origin, which were present in negligible amounts following each passage but then grew and formed a basal, feeder layer. Throughout a culture period of over 2 years, the L3 cells have maintained a stable morphological and antigenic phenotype. In serum-containing culture medium, most of the process-bearing cells expressed at the same time features of immature oligodendrocytes (O4 positivity) and of astrocytes [glial fibrillary acidic protein (GFAP) positivity]. A smaller proportion of them was labeled by the monoclonal antibody LB1. LB1+ or O4+ cells were rarely GFAP-, and GFAP+ cells were rarely LB1- or O4-. GalC+ oligodendrocytes were seen only occasionally, but the proportion of these cells increased up to 30% upon culturing in chemically defined medium containing 0.5% fetal calf serum. The L3 process-bearing cells accumulated the neurotransmitter gamma-aminobutyric acid (GABA), expressed the proteoglycan chondroitin sulfate, and responded to the mitogenic action of platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF). All these properties are characteristic of cells belonging to the O-2A (oligodendrocyte-type 2 astrocyte) cell lineage. The L3 flat cells were largely negative for the glial markers tested, but resembled type 1 astrocytes in their ability to support the growth of O-2A lineage cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Modulation of non-N-methyl-D-aspartate receptors in cultured cerebellar granule cells.

Kainic acid (KA), quisqualic acid (QUIS), and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) stimulated D-[3H]aspartate release from cultured cerebellar granule cells in a concentration-dependent way. The EC50 values were 50 microM for KA (Gallo et al., 1987) and 20 microM for both QUIS and AMPA, but the efficacy of QUIS appeared to be greater than that of AMPA. The release of D-[3H]aspartate induced by KA, QUIS, and AMPA was blocked, in a dose-dependent way, by the new glutamate receptor antagonist 6-cyano-2,3-dihydroxy-7-nitroquinoxaline (CNQX); IC50 values were 0.7 microM in the case of AMPA (50 microM) and 1 microM in the case of KA (50 microM). AMPA (50-300 microM) inhibited the effect of 50 microM KA on D-[3H]aspartate release. At 300 microM AMPA, the effect of KA plus AMPA was not antagonized by the KA receptor antagonist kynurenic acid (KYN). In contrast, when KA was used at an ineffective concentration (10 microM), the addition of AMPA at concentrations below the EC50 value (10-20 microM) resulted in a synergistic effect on D-[3H]aspartate release. In this case, the evoked release of D-[3H]aspartate was sensitive to KYN. KA stimulated the formation of cyclic GMP, whereas QUIS, AMPA, and glutamate were ineffective. The accumulation of cyclic GMP elicited by KA (100 microM) was prevented not only by the antagonists CNQX (IC50 = 1.5 microM) and KYN (IC50 = 200 microM), but also by the agonists AMPA (IC50 = 50 microM) QUIS (IC50 = 3.5 microM), and glutamate (IC50 = 100 microM). We conclude that AMPA, like QUIS, may act as a partial agonist at KA receptors. Moreover, CNQX effectively antagonizes non-N-methyl-D-aspartate receptor-mediated responses in cultured cerebellar granule cells.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1990

Thyroxine-dependent modulations of the expression of the neural cell adhesion molecule N-CAM during Xenopus laevis metamorphosis.

During amphibian metamorphosis, a complete remodeling of the phenotype takes place under complex hormonal control whose final effectors are thyroid hormones. This process implies the activation of coordinated programs of cell death, proliferation, migration, adhesion and differentiation. Inasmuch as the neural cell adhesion molecule N-CAM is thought to play a central role in the control of morphogenetic processes, we have studied by immunohistofluorescence and immunoblots the patterns of expression of N-CAM at different stages of Xenopus laevis metamorphosis. A scan was made of all major organs and appendages. Before the metamorphic climax, all neuronal cell bodies and processes express high levels of N-CAM. During the metamorphic climax, N-CAM expression decreases sharply on the cell bodies and processes of the peripheral nervous system (PNS) but remains high in the central nervous system (CNS). Towards the end of metamorphosis, the PNS and spinal nerves are virtually negative for N-CAM while the CNS is still positive. The optic and olfactory nerves, although myelinated, are still strongly positive for N-CAM. The lens and olfactory epithelia express N-CAM throughout metamorphosis. In the brain. N-CAM is present at all times as three polypeptides of 180, 140, and 120 X 10(3) Mr; before metamorphosis some of the N-CAM is in its polysialylated form. During metamorphosis and the subsequent growth of the animal, the amount of N-CAM decreases gradually. In all polypeptides, the polysialylated form is the first to disappear. Cardiac muscle expresses high level of N-CAM from its first formation throughout metamorphosis; in contrast, the level of N-CAM in skeletal muscle is high in newly formed muscles, but decreases rapidly after myoblast fusion. The liver of adult Xenopus contains large amounts of a 160 X 10(3) polypeptide that is recognized by polyclonal and monoclonal antibodies against N-CAM. cDNA probes of Xenopus brain N-CAM recognize major transcripts of 9.2, 3.8 and 3.3 kb in Xenopus liver mRNA; these bands are different in size from those recognized in brain mRNA (9.5, 4.2 and 2.2 kb). Premetamorphic liver does not express the 160 X 10(3) form of N-CAM, which can be first detected at stage 59 and persists then through all the life of the animal. Expression of N-CAM in the liver can be induced in premetamorphic animals (stage 51-52) by a 48 h treatment with thyroxine. All hepatocytes are responsive.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Measurement of amino acid release from cultured cerebellar granule cells by an improved high performance liquid chromatography procedure.

Endogenous amino acid release was examined in rat cerebellar primary cultures comprising more than 95% of glutamatergic granule cells. Eighteen amino acids were determined in the cell extracts and in the release fractions by high performance liquid chromatography, using precolumn derivatization with o-phthaldialdehyde and separation on a reverse-phase column using a multi-step gradient system of two solvents (0.1 M Na+ acetate, pH 7.2/methanol: tetrahydrofuran, 97:3). The fluorimetric response was linear, at least in the range of 2-162 pmol, for all the amino acids analysed, with a detection limit of 1 pmole. We observed a good reproducibility in within-assay and between-assay coefficients of variation of the retention times and fluorescence yield. When cultured granule cells were exposed to the excitatory amino acid receptor agonist quisqualic acid (50 microM), we observed a net increase in the release of glutamate (3 fold over the baseline) and a smaller increase in that of aspartate (2 fold) and taurine (1.6 fold). Other amino acids were not significantly affected. GABA levels were below detection limits, due to the minimal number of GABAergic neurons present in the cultures.

Amino Acids↗
PubMed1989

Expression of excitatory amino acid receptors by cerebellar cells of the type-2 astrocyte cell lineage.

We have used postnatal rat cerebellar astrocyte-enriched cultures to study the excitatory amino acid receptors present on these cells. In the cultures used, type-2 astrocytes (recognized by the monoclonal antibodies A2B5 and LB1) selectively took up gamma-[3H]aminobutyric acid ([3H]GABA) and released it when incubated in the presence of micromolar concentrations of kainic and quisqualic acids. The releasing effect of kainic acid was concentration dependent in the range of 5-100 microM. Quisqualate was more effective than kainate in the lower concentration range but less effective at concentrations at which its releasing activity was maximal (approximately 50 microM). N-Methyl-D-aspartic acid and dihydrokainate (100 microM) did not stimulate [3H]GABA release from cultured astrocytes. L-Glutamic acid (20-100 microM) stimulated [3H]GABA release as effectively as kainate. The stimulatory effects of kainate and quisqualate on [3H]GABA release were completely Na+ dependent; that of kainate was also partially Ca2+ dependent. Kynurenic acid (50-200 microM) selectively antagonized the releasing effects of kainic acid and also that of L-glutamate; quisqualate was unaffected. Quisqualic acid inhibited the releasing effects of kainic acid when both agonists were used at equimolar concentrations (50 microM). D-[3H]aspartate was taken up by both type-1 and type-2 astrocytes, but only type-2 astrocytes released it in the presence of kainic acid. Excitatory amino acid receptors with a pharmacology similar to that of the receptors present in type-2 astrocytes were also expressed by the immature, bipotential progenitors of type-2 astrocytes and oligodendrocytes.

Animals↗
PubMed1989

Quisqualic acid modulates kainate responses in cultured cerebellar granule cells.

The activation of kainic acid and quisqualic acid receptors in cultured cerebellar granule cells stimulated the release of preaccumulated D-[3H]aspartate. The effect of kainate could be distinguished from that of quisqualate by its sensitivity to the antagonists kynurenic acid and 2,3-cis-piperidine dicarboxylic acid. At a concentration of kainic acid (50 microM) close to its half-maximal releasing effect, simultaneous addition of quisqualic acid (10-50 microM) resulted in a significant dose-dependent inhibition of the kainate-induced component of D-[3H]aspartate release, which was monitored by the progressive decrease in sensitivity of the evoked release to kynurenic acid. In contrast, when kainic acid was used at a subeffective concentration (10 microM), addition of low doses of quisqualate (2-5 microM) resulted in a synergistic effect on D-[3H]aspartate release. Under these conditions, the effect of the two agonists was sensitive to kynurenic acid. Kainic acid (50-100 microM) also caused a dose-dependent, kynurenic acid-sensitive accumulation of cyclic GMP (cGMP) in granule cell cultures. Quisqualic acid was, by itself, ineffective and prevented, in a dose-dependent manner, the kainate-induced cGMP formation (IC50 = 5 microM). Finally, the guanylate cyclase activator sodium nitroprusside greatly enhanced cGMP formation but had no effect on D-[3H]aspartate release. Together, these results demonstrate the existence of complex interactions between quisqualic and kainic acids and indicate that the effects of the two glutamate agonists on D-[3H]aspartate release and on cGMP accumulation are independent.

Animals↗
PubMed1989

Patterns of expression of a 15K beta-D-galactoside-specific lectin during early development of the avian embryo.

We have determined, by immunohistochemical and biochemical techniques, the distribution of an endogenous beta-D-galactoside-binding lectin between the early primitive streak stage and the 5th day of embryonic development of the chick. The lectin, which was purified from the pectoral muscle of 16-day-old chick embryos, migrates on SDS-PAGE as a single polypeptide of relative molecular mass 15 x 10(3). Antibodies to this pure lectin interact with the 15K (K = 10(3) M(r)) polypeptide as well as with a 6.5K polypeptide; this second component appears to be antigenically related to the 15K lectin, as antibodies affinity purified on the 15K band recognize both polypeptides. In early stages of development, lectin immunoreactivity was present in most cells of the epiblast and hypoblast in the region of the primitive streak, while towards the edge of the area pellucida the epiblast was stained less intensely. During gastrulation, strong immunoreactivity was present also in migrating cells and in the mesoblast, while at the margin of the area pellucida the epiblast was negative. Up to the 10-somite stage, lectin immunoreactivity was present in the somites, neural tube and presumptive cardiac region; the non-neural ectoderm and the extracellular matrix were not labeled; the predominant immunoreactive component at this stage of development was the 6.5K polypeptide. Later in development, the lectin immunoreactivity gradually disappeared from the dermamyotome and nervous system to reappear conspicuously as soon as a differentiated myotome could be detected. Immunoreactivity was very high in the myotome, skeletal and cardiac muscles and transient in smooth muscles. The only region of the nervous system that continued to express the lectin throughout development was the trigeminal (semilunar) ganglion; in all regions of the nervous system, the lectin immunoreactivity disappeared early in development to be re-expressed only much later. The lining epithelium of the digestive tract and other endodermal derivatives expressed the lectin transiently. In the extraembryonic membranes, immunoreactivity to the lectin was observed in the yolk sac and in both layers of the amnion. The striking regulation of the expression of this endogenous lectin suggests that its functions are linked to cell proliferation and/or to the selective expression of a developmentally-timed cell phenotype.

Animals↗
PubMed1988

Differentiation of bipotential glial precursors into oligodendrocytes is promoted by interaction with type-1 astrocytes in cerebellar cultures.

The differentiation of bipotential precursors of oligodendrocytes (OL) and type-2 astrocytes (AS) was followed in primary cultures from 8-day postnatal rat cerebellum by labeling the cells with the antibodies LB1 (which binds to the surface disialoganglioside GD3 present in glial precursors, type-2 AS, and immature OL), O4 (a marker of immature and mature OL binding to surface sulfatide), anti-galactocerebroside (GalCer, a marker of OL), and anti-glial fibrillary acidic protein (GFAP, a marker of AS). Two hours after plating, hardly any LB1+, GFAP+ cells were detectable, 40% of the O4+ cells were GalCer+, and none of the O4+ cells were GFAP+. Upon culturing cells plated at a density of 1 x 10(5) cells per cm2 in the presence of fetal calf serum, most of the LB1+ precursors differentiated into type-2 AS, even if most of them had already expressed the O4 antigen. Thus, in culture, most type-2 AS seem to derive from progenitor cells that were differentiating in vivo into OL. In higher density cultures (2.5 x 10(5) cells per cm2), however, many precursors differentiated into GalCer+ OL, rather than into AS. As a possible source of the signals responsible for the behavior of the glial precursors in high-density cultures, we focused our attention on type-1 AS, the most abundant cell type in the cultures. We found that, in low-density cultures maintained for 5-7 days in a medium conditioned by type-1 AS, the proliferation of the precursors was enhanced and their differentiation into OL or AS was prevented. In contrast, when cerebellar cells were coplated with type-1 AS dissociated from purified cultures, not only did the precursors proliferate more than in control cultures, but also a larger proportion of them differentiated into GalCer+ OL. In conclusion, type-1 AS appear to facilitate the differentiation of bipotential glial precursors into OL through direct cell-cell interactions. The influence of type-1 AS on the differentiation of the LB1+ and O4+ precursors is supported also by experiments with glial cortical cultures.

Animals↗
PubMed1988

Distribution and role in regeneration of N-CAM in the basal laminae of muscle and Schwann cells.

The neural cell adhesion molecule (N-CAM) is a membrane glycoprotein involved in neuron-neuron and neuron-muscle adhesion. It can be synthesized in various forms by both nerve and muscle and it becomes concentrated at the motor endplate. Biochemical analysis of a frog muscle extract enriched in basal lamina revealed the presence of a polydisperse, polysialylated form of N-CAM with an average Mr of approximately 160,000 as determined by SDS-PAGE, which was converted to a form of 125,000 Mr by treatment with neuraminidase. To define further the role of N-CAM in neuromuscular junction organization, we studied the distribution of N-CAM in an in vivo preparation of frog basal lamina sheaths obtained by inducing the degeneration of both nerve and muscle fibers. Immunoreactive material could be readily detected by anti-N-CAM antibodies in such basal lamina sheaths. Ultrastructural analysis using immunogold techniques revealed N-CAM in close association with the basal lamina sheaths, present in dense accumulation at places that presumably correspond to synaptic regions. N-CAM epitopes were also associated with collagen fibrils in the extracellular matrix. The ability of anti-N-CAM antibodies to perturb nerve regeneration and reinnervation of the remaining basal lamina sheaths was then examined. In control animals, myelinating Schwann cells wrapped around the regenerated axon and reinnervation occurred only at the old synaptic areas; new contacts between nerve and basal lamina had a terminal Schwann cell capping the nerve terminal. In the presence of anti-N-CAM antibodies, three major abnormalities were observed in the regeneration and reinnervation processes: (a) regenerated axons in nerve trunks that had grown back into the old Schwann cell basal lamina were rarely associated with myelinating Schwann cell processes, (b) ectopic synapses were often present, and (c) many of the axon terminals lacked a terminal Schwann cell capping the nerve-basal lamina contact area. These results suggest that N-CAM may play an important role not only in the determination of synaptic areas but also in Schwann cell-axon interactions during nerve regeneration.

Animals↗
PubMed1988

Coxsackie virus heart disease: 15 years after.

From 1969 to 1973, 68 patients were admitted to the 4th Division of Medicine of the Brescia Civil Hospital with the diagnosis of viral myocarditis. The patients were divided into two groups according to the results of the Coxsackie virus complement fixing antibodies test: Group 1 (42 patients) with a fourfold or greater rising antibody titre; Group 2 (26 patients) with a negative serum test. Both groups were examined after a follow-up period of 15 years. Ten patients from Group 1 died. The diagnoses were chronic myocarditis (three cases); chronic cardiomyopathy-pulmonary embolism (one case); chronic cardiomyopathy-liver cirrhosis (one case); dilated cardiomyopathy-sudden death (two cases); congestive cardiomyopathy (three cases). No Group 2 patients died. The 15-year mortality rate of Group 1 was significantly higher than that of Group 2 (Fisher Test: p less than 0.005). In conclusion, the natural history of Coxsackie virus heart disease is characterized by two possibilities: a complete recovery from a clinical point of view, in some cases with only minor T wave abnormalities, or evolution into a chronic disease (dilated cardiomyopathy) having a high mortality rate within 10 years of the onset of the acute disease.

Cardiomyopathy, Dilated↗
PubMed1988

Noninvasive assessment of pulmonary hypertension: a simultaneous echo-Doppler hemodynamic study.

Thirty patients with stable chronic obstructive lung disease (COLD) underwent an echo-Doppler examination before and during right heart catheterization. No statistically significant differences between observations for any of two-dimensional echo-Doppler parameters were found. The measurement of all parameters taken during the catheterization correlated better with mean pulmonary artery pressure (mPAP) than those taken before. This difference was most evident for the isovolumetric acceleration time (r = 0.71 before versus r = 0.85 during the catheterization) and relaxation time (r = -0.75 before versus r = -0.87 during the catheterization). The multiple correlation coefficient for all measured parameters and mPAP was 0.83 before and 0.92 during the catheterization. In conclusion, in patients with COLD, it appears possible to get reliable information about PAP using noninvasive techniques.

Adult↗
PubMed1987

Functional evaluation of glutamate receptor subtypes in cultured cerebellar neurones and astrocytes.

Micromolar concentrations of kainic acid and quisqualic acid released [3H]D-aspartate preaccumulated by cerebellar granule cells in culture. The effect of kainate was selectively antagonized by kynurenic acid and, less effectively, by PDA. Kainate and quisqualate also increased [3H]GABA release from a subpopulation of cultured cerebellar astrocytes. Kynurenic acid selectively blocked the effect of kainic acid. NMDA and no D-aspartate or GABA releasing effect. These results suggest the existence of two different excitatory amino acid sites active on neurotransmitter amino acid release in both cerebellar granule cells and astrocytes.

Amino Acids↗
PubMed1987

Differentiation of cerebellar bipotential glial precursors into oligodendrocytes in primary culture: developmental profile of surface antigens and mitotic activity.

We have analyzed the changes in surface antigenic properties of cerebellar bipotential precursors of oligodendrocytes and type-2 astrocytes during their differentiation into oligodendrocytes in serum-free cultures and the relationship between antigen expression and proliferation of these cells. Double immunofluorescence experiments with different monoclonal antibodies (mabs) performed at various stages in vitro and immunocytolysis experiments provided evidence for the following antigenic developmental profile: at early stages in culture the progenitor cells are recognized by the mabs A2B5 and LB1 (which bind to surface gangliosides) but not by other mabs known to label immature or mature oligodendrocytes (04, 01, and anti-galactocerebroside [GalC]). A few days later, the precursors start to express the 04 antigen; at this stage they maintain a bipotential nature and, in the presence of serum, they differentiate into type-2 astrocytes. If maintained in serum-free medium, the progenitor cells enter the oligodendrocyte differentiation compartment, acquiring GalC positivity. Soon after becoming GalC+, the cells lose both bipotentiality and the surface antigens binding A2B5 and LB1. They conserve, however, the antigen binding 04. Experiments of [3H]thymidine autoradiography combined with immunofluorescence showed that a greater proportion of the LB1+ cells incorporated the radioactive nucleoside into their nuclei as compared to the 04+ cells. No incorporation was present in GalC+ oligodendrocytes.

Animals↗