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  • 1
    Electronic Resource
    Electronic Resource
    Expression of potassium channels during postnatal differentiation of rabbit Müller glial cells (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The postnatal maturation of Müller glial cells from immature radial glial cells is accompanied by specific changes in the activity of distinct types of K+ channels, as shown by whole-cell and cell-attached records on freshly isolated cells from retinae of young (postnatal days 1–30, P1–P30) and adult rabbits. (i) The density of inwardly rectifying currents, providing the main K+ conductance in adult Müller cells, was very low (0.8 pA/pF) from P1 to P6 but increased rapidly thereafter until a relatively stable level of 11.0 pA/pF was established at P17. (ii) Transient (A-type) K+ currents were expressed in all immature cells at a high density (9.6 pA/pF). After P12, both the percentage of cells with A-type currents and the peak amplitudes of the currents (2.8 pA/pF) declined. (iii) Delayed rectifying K+ currents developed slowly until after P30. (iv) The postnatal maturation of radial glial cells was accompanied by a strong decrease in the activity of large-conductance, Ca2+-activated K+ channels, the open probability of which (measured at the resting membrane potential) decreased from 0.69 at P2–4 to 0.06 at P13–14. The developmental decrease of the activity of Ca2+-activated K+ channels is assumed to be mainly caused by alteration of the resting membrane potential which developed from low values (–49 mV) at P1–6 to high adult values (–84 mV) after P13. The activity of each distinct type of K+ channel investigated is differently modulated by developmental regulation. This may reflect different functional requirements of immature and mature Müller cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00706.x
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  • 2
    Electronic Resource
    Electronic Resource
    Retinal gliopathy accompanying thioacetamide-induced liver insufficiency: light and electron microscopic observations (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 57-66 
    Details
    ISSN: 1432-0533
    Keywords: Key words Rat ; Thioacetamide ; Liver insufficiency ; Hepatic encephalopathy ; Müller glia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A recent examination of retinae of patients who had died with symptoms of liver insufficiency (LI) including hepatic encephalopathy (HE) revealed morphological changes in retinal Müller glia similar to the astrocytic changes normally accompanying HE, and the term “hepatic retinopathy” (HR) was coined to define these changes. In the present study, the immunomorphology and ultrastructure of Müller cells were examined in rats in which LI with accompanying HE was induced with a hepatotoxin, thioacetamide (TAA). Light microscopically, retinae of rats with LI were characterized by swelling of the Müller cell cytoplasm. Immunostaining for glia-specific marker proteins in Müller cells from LI rats revealed a strongly enhanced expression of glial fibrillary acidic protein, and a considerable increase in glutamine synthetase immunoreactivity, as compared to control animals. Ultrastructurally, the Müller cells of LI rats showed swelling and vacuolization of cell processes. In particular, the endfeet contained many swollen mitochondria. By contrast, LI produced no morphologically demonstrable changes in retinal neurons and photoreceptor cells. Thus, the retinal changes induced by TAA in the rats strongly resembled those described in human HR, rendering the present rat model suitable for more detailed investigations of the pathomechanism(s) of HR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050860
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  • 3
    Electronic Resource
    Electronic Resource
    Hepatic retinopathy: morphological features of retinal glial (Müller) cells accompanying hepatic failure (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 273-281 
    Details
    ISSN: 1432-0533
    Keywords: Ammonia ; Glia ; Retina ; Morphometry ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract More than 80 years ago, Alzheimer described changes in the brains of patients who had suffered hepatic failure. Astrocytes are primarily affected; their nuclei become swollen, their intermediate filament protein composition is altered and their cytoplasm becomes vacuolated. Cells with these features are called Alzheimer type II astrocytes and these changes have been attributed to the toxic effects of elevated ammonia levels. The present study investigates whether the dominant glia of another part of the central nervous system, the Müller cells of the retina, undergo similar changes. Retinae of patients who had died with symptoms of hepatic failure were processed for histology, histochemistry, and immunocytochemistry. Cell nuclei were measured from brain astrocytes (insula cortex), Müller cells, and retinal bipolar neurons. Hepatic failure resulted in the enlargement of nuclei in astrocytes and Müller cells, and the enhanced expression in Müller cells of glial fibrillary acidic protein, cathepsin D, and the β-subunit of prolyl 4-hydroxylase (glial-p55). In some retinae, signs of gliosis were also observed. We conclude that increased levels of serum ammonia resulting from hepatic insufficiency cause changes in Müller cells that are similar to those seen in brain astrocytes. We term this condition hepatic retinopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296511
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  • 4
    Electronic Resource
    Electronic Resource
    Hepatic retinopathy: morphological features of retinal glial (Müller) cells accompanying hepatic failure (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 273-281 
    Details
    ISSN: 1432-0533
    Keywords: Key words Ammonia ; Glia ; Retina ; Morphometry ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract More than 80 years ago, Alzheimer described changes in the brains of patients who had suffered hepatic failure. Astrocytes are primarily affected; their nuclei become swollen, their intermediate filament protein composition is altered and their cytoplasm becomes vacuolated. Cells with these features are called Alzheimer type II astrocytes and these changes have been attributed to the toxic effects of elevated ammonia levels. The present study investigates whether the dominant glia of another part of the central nervous system, the Müller cells of the retina, undergo similar changes. Retinae of patients who had died with symptoms of hepatic failure were processed for histology, histochemistry, and immunocytochemistry. Cell nuclei were measured from brain astrocytes (insula cortex), Müller cells, and retinal bipolar neurons. Hepatic failure resulted in the enlargement of nuclei in astrocytes and Müller cells, and the enhanced expression in Müller cells of glial fibrillary acidic protein, cathepsin D, and the β-subunit of prolyl 4-hydroxylase (glial-p55). In some retinae, signs of gliosis were also observed. We conclude that increased levels of serum ammonia resulting from hepatic insufficiency cause changes in Müller cells that are similar to those seen in brain astrocytes. We term this condition hepatic retinopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296511
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  • 5
    Electronic Resource
    Electronic Resource
    Development of the neonatal rabbit retina in organ culture (1997)
    Springer
    Anatomy and embryology 196 (1997), S. 67-79 
    Details
    ISSN: 1432-0568
    Keywords: Key words In vitro development ; Proliferation ; Differentiation ; Glia ; Müller cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Organ cultures from neonatal rabbit retinae grew well over periods of up to 2 weeks in vitro. Proliferation in vitro declined in parallel with the decline seen in vivo, although the rate of proliferation in the explants was slightly reduced. The proliferation of progenitor cells in vitro produced the same cell types produced postnatally in vivo. Postnatally generated cell clones, labeled by means of a retroviral vector, consisted mainly of rods and Müller cells. The layers of the retinae developed as in vivo; an outer plexiform layer occurreed after the first 2 days in vitro. Ultrastructurally, ribbon synapses (outer and inner plexiform layer) and conventional synapses (inner plexiform layer) were observed. The photoreceptor cells grew well-developed inner segments and cilia but no mature outer segments. The cultured retinae contained a well-developed, regular lattice of Müller cells expressing vimentin as in vivo. The neuron-to-Müller cell-ratios were essentially the same as in vivo, viz. about 15 to 16 neurons, among them about 10 to 11 (rod) photoreceptor cells per Müller cell. When the glia cell-specific toxin α-aminoadipic acid (αAAA) was applied, the pattern of vimentin-positive Müller cells became irregular, or even locally missing. In such cases, the tissue became disorganized as indicated by a local disappearance of the regular layering, and development of many rosettes. It is concluded that an intact lattice of Müller cells is necessary for the migration of young neurons, and for correct formation of retinal layers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004290050080
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  • 6
    Electronic Resource
    Electronic Resource
    Distribution of mitochondria within Muller cells – II. Post-natal development of the rabbit retinal periphery in vivo and in vitro: dependence on oxygen supply (1998)
    Springer
    Journal of neurocytology 27 (1998), S. 347-359 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The occurrence and localization of mitochondria within glial (Muller) cells and neurons of the peripheral (avascular) rabbit retina was studied electron microscopically and by immunocytochemical demonstration of the mitochondrial enzyme GABA transaminase (GABA-T). Post-natal development in vivo was compared with development of organ cultures from neonatal rabbit retinae, grown over 2 weeks in vitro. The adult pattern of mitochondrial localization (restriction to the sclerad end of the cells) was observed from the beginning of enzyme expression at early post-natal stages. However, when neonatal retinal pieces were grown in vitro with their vitread surface exposed to the air, their Muller cells contained mitochondria along most of their length. When functionally developed retinae from postnatal day 14 were explanted in vitro, they retained their sclerad mitochondrial distribution for almost 24 h but thereafter the inner portions of their cytoplasm became occupied by mitochondria within a few hours. This was achieved mainly by mitochondrial migration rather than by formation of new mitochondria because it was not prevented by cycloheximide-induced inhibition of protein synthesis. These data support the following hypotheses: (1) the mitochondrial distribution in Muller cells is determined by the local cytoplasmic O2 pressure (pO2), (2) existing mitochondria move towards cytoplasmic regions of sufficient pO2 by rather rapid migration and (3) the start of this migration is delayed by almost 24 h due to the action of as yet unknown control mechanisms. In contrast, the mitochondrial content of retinal ganglion and amacrine cells in the vitread retinal layers was virtually independent of the source and level of oxygen supply.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006938825474
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  • 7
    Electronic Resource
    Electronic Resource
    Alterations of Müller (glial) cells in dystrophic retinae of RCS rats (1995)
    Springer
    Journal of neurocytology 24 (1995), S. 507-517 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have carried out a light microscopical study of Müller cells in the retinae of rats with inherited retinal dystrophy (Royal College of Surgeons rats). Isolated retinae of both control and Royal College of Surgeons rats were exposed to a Procion Yellow solution which is taken up selectively into Müller cells. The shape of the cells was then studied by confocal microscopy. Enzymatically isolated Müller cells were studied immunocytochemically with antibodies against glial fibrillary acidic protein, cathepsin D, β-amyloid precursor protein, bcl-2 protooncogene product, and glutamine synthetase. Müller cells from RCS retinae were shorter than those from control retinae, and showed a coarse hypertrophy of their distal (sclerad) processes. In Müller cells isolated from the retinae of Royal College of Surgeon's rats, the expression of glial fibrilliary acidic protein, cathepsin D, β-amyloid precursor protein and bcl-2 protooncogene product was increased, and the expression of glutamine synthetase was reduced. Obviously, loss of neighbouring neurons leads to major alterations of both the shape and metabolism of Müller cells. The expression of enzymes that serve functional glio-neuronal interactions, such as glutamine synthetase, seems to be down-regulated, whereas proteins involved in cell reconstruction (cathepsin D), cell repair (possibly β-amyloid precursor protein), and protection against apoptotic cell death (bcl-2 protooncogene product), are up-regulated, together with the ‘pathological marker’ glial fibrilliary acidic protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01179976
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  • 8
    Electronic Resource
    Electronic Resource
    Comparative studies on mammalian Muller (retinal glial) cells (1997)
    Springer
    Journal of neurocytology 26 (1997), S. 439-454 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Muller cells from 22 mammalian species were subjected to morphological and electrophysiological studies. In the ‘mid-periphery’ of retinae immunocytochemically labeled for vimentin, estimates of Muller cell densities per unit retinal surface area, and of neuron-to-(Muller) glia indices were performed. Muller cell densities were strikingly similar among the species studied (around 8000–11000 mm−2) with the extremes of the horse (≤5000 mm−2) and the tree shrew (≥20000 mm−2). By contrast, the number of neurons per Muller cell varied widely, being clustered at 6–8 (in retinae with many cones), at about 16, and at up to more than 30 (in strongly rod-dominated retinae). Isolated Muller cell volumes were estimated morphometrically, and cell surface areas were calculated from membrane capacities. Muller cells isolated from thick vascularized retinae (carnivores,rats, mice, ungulates) were longer and thinner, and had smaller volumes but higher surface-to-volume ratios than cells from thin paurangiotic (i.e. with blood vessels only near the optic disc) or avascular retinae (rabbits, guinea pigs, horses, zebras). In whole-cell voltage-clamp studies, Muller cells from all mammals studied displayed two dominant K+ conductances, inwardly rectifying currents and delayed rectifier currents. TTX-sensitive Na+ currents were recorded only in some species. Based on these data, the following hypotheses are presented, (a) neuron-to-(Muller) glia indices are determined by precursor cell proliferation rather than by metabolic demands; (b) Muller cell volumes depend on available space rather than on the number of supported neurons; and (c) it follows that, the specific metabolic activities of Muller cells must differ greatly between species, a difference that may contribute to distinct patterns of retinal vascularization.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018525222826
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  • 9
    Electronic Resource
    Electronic Resource
    Distribution of mitochondria within Muller cells – I. Correlation with retinal vascularization in different mammalian species (1998)
    Springer
    Journal of neurocytology 27 (1998), S. 329-345 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The distribution of mitochondria within retinal glial (Muller) cells and neurons was studied by electron microscopy, by confocal microscopy of a mitochondrial dye and by immunocytochemical demonstration of the mitochondrial enzyme GABA transaminase (GABA-T). We studied sections and enzymatically dissociated cells from adult vascularized (human, pig and rat) and avascular or pseudangiotic (guinea-pig and rabbit) mammalian retinae. The following main observations were made. (1) Muller cells in adult euangiotic (totally vascularized) retinae contain mitochondria throughout their length. (2) Muller cells from the periphery of avascular retinae display mitochondria only within the sclerad-most end of Muller cell processes. (3) Muller cells from the vascularized retinal rim around the optic nerve head in guinea-pigs contain mitochondria throughout their length. (4) Muller cells from the peripapillar myelinated region (‘medullary rays’) of the pseudangiotic rabbit retina contain mitochondria up to their soma. In living dissociated Muller cells from guinea-pig retina, there was no indication of low intracellular pH where the mitochondria were clustered. These data support the hypothesis that Muller cells display mitochondria only at locations of their cytoplasm where the local O2 pressure (pO2) exceeds a certain threshold. In contrast, retinal ganglion cells of guinea-pig and rabbit retinae display many mitochondria although the local pO2 in the inner (vitread) retinal layers has been reported to be extremely low. It is probable that the alignment of mitochondria and the expression of mitochondrial enzymes are regulated by different mechanisms in various types of retinal neurons and glial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006934724566
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