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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Excitatory ATP responses in rat cultured thoracolumbar sympathetic neurones are mediated by somatic P2X2 receptors. The present study investigated a possible role of axonal P2X2 as well as P2X7 receptors on the same preparation. Confocal laser scanning microscopy demonstrated P2X2 and P2X7 immunoreactivity along the axons as well as P2X7 immunoreactivity surrounding the cell nuclei. P2X7 mRNA expression was detected in individual neurones using a single-cell RT–PCR approach. Adenosine triphosphate (ATP) caused a significant increase in axonal Ca2+ concentration which was dependent on external Ca2+ but insensitive to depletion of the cellular Ca2+ pools by cyclopiazonic acid. Pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonate (PPADS; 30 µm) virtually abolished the ATP response, whereas brilliant blue G (0.1 µm), a selective P2X7 receptor antagonist, had no effect. Dibenzoyl-ATP (BzATP; 100 µm) induced a much smaller increase in axonal [Ca2+] concentration than ATP at equimolar concentrations. The response to BzATP was distinctly reduced by PPADS but not by brilliant blue G. The overall pharmacological profile of the axonal P2X receptors resembled closely that of the somatic P2X2 receptors. In conclusion, the present data suggest the occurrence of axonal excitatory P2X2 receptors in thoracolumbar sympathetic neurones. However, the functional significance of axonal and (peri)-nuclear P2X7 receptors has still to be proven.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Berlin, Germany : Blackwell Verlag GmbH
    Anatomia, histologia, embryologia 34 (2005), S. 0 
    ISSN: 1439-0264
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Borna disease virus (BDV) causes a non-purulent meningoencephalitis and retinitis in a variety of species. In Lewis rats infected intracerebrally with the highly neurotropic BDV the retina is one of the most severely affected central nervous system (CNS) structures. While BDV-induced damage in the brain has previously been shown to be caused by a T-cell-dependent process, the immunopathological mechanisms leading to BDV-induced retinitis, remain to be elucidated. RNA samples from retinae were subjected to RNase protection assays to detect transcripts of proinflammatory cytokines and chemokines known to be involved in the recruitment of T-cells and macrophages in the CNS. The observed expression profile of proinflammatory cytokines and chemokines, as well as the immunohistochemical detection of αβTCR-positive and CD8-positive T-cells in the BDV-infected retinae, is reminiscent of the situation observed in the brains of Lewis rats during the acute phase of Borna disease. This suggests, that similar immunopathological mechanisms are operating in retinae and brains of infected rats. This research was supported by grants from the Deutsche Forschungsgemeinschaft (J.S.-PA 615/1-1).
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The present study investigated the pharmacological properties of excitatory P2X receptors and P2X2 and P2X5 receptor subunit expression in rat-cultured thoracolumbar sympathetic neurons. In patch-clamp recordings, ATP (3–1000 µm; applied for 1 s) induced inward currents in a concentration-dependent manner. Pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonate (PPADS; 30 µm) counteracted the ATP response. In contrast to ATP, α,β-meATP (30 µm; for 1 s) was virtually ineffective. Prolonged application of ATP (100 µm; 10 s) induced receptor desensitization in a significant proportion of sympathetic neurons in a manner typical for P2X2−2 splice variant-mediated responses. Using single-cell RT-PCR, P2X2, P2X2−2 and P2X5 mRNA expression was detectable in individual tyrosine hydroxylase-positive neurons; coexpression of both P2X2 isoforms was not observed. Laser scanning microscopy revealed both P2X2 and P2X5 immunoreactivity in virtually every TH-positive neuron. P2X2 immunoreactivity was largely distributed over the cell body, whereas P2X5 immunoreactivity was most distinctly located close to the nucleus. In summary, the present study demonstrates the expression of P2X2, P2X2−2 and P2X5 receptor subunits in rat thoracolumbar neurons. The functional data in conjunction with a preferential membranous localization of P2X2/P2X2−2 compared with P2X5 suggest that the excitatory P2X responses are mediated by P2X2 and P2X2−2 receptors. Apparently there exist two types of P2X2 receptor-bearing sympathetic neurons: one major population expressing the unspliced isoform and another minor population expressing the P2X2−2 splice variant.
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  • 5
    ISSN: 0898-6568
    Keywords: DNA synthesis ; K-ATPase activity ; Na ; Potassium ; arginine-vasopressin ; cell culture ; epithelial growth factor ; neuroglia ; protein synthesis
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Graefe's archive for clinical and experimental ophthalmology 216 (1981), S. 245-251 
    ISSN: 1435-702X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Quantitative Untersuchungen des Zellbesatzes der Netzhaut von Diabetikern und Stoffwechselgesunden gleicher Alters- und Geschlechtsverteilung werden vorgelegt. Bereits bei einer Diabetesdauer bis zu 6 Jahren finden sich im zentralen Netzhautbereich drastische Verminderungen der Zellzahlen in der Ganglienzellschicht. Zu diesem Zeitpunkt sind die Zellzahlen in der inneren Körnerschicht der zentralen Retina gering und in der äußeren Körnerschicht gar nicht vermindert. Die periphere Netzhaut von Diabetikern mit kurzer Krankheitsdauer weist einen unveränderten Zellbesatz aller Schichten auf. Bei längerer Diabetesdauer (über 10 Jahre) finden sich signifikante Verminderungen der Zellzahlen in allen Schichten sowohl zentral als auch peripher. Die beobachteten Zellausfälle werden auf Störungen der retinalen Mikrozirkulation zurückgeführt. Bei relativ geringer Diabetesdauer sind Störungen im Bereich der A. centralis retinae bekannt, bei Langzeitdiabetes wird auch die Choriocapillaris betroffen. Es werden Zusammenhänge zwischen dem Muster der Zellausfälle und den funktionellen (elektroretinographischen) Befunden diskutiert.
    Notes: Abstract A quantitative exploration of retinal cell content was carried out in diabetics and metabolically healthy controls of the same age and sex distribution. After diabetes of 6 years duration there was a drastic diminution of cells in the ganglion cell layer of the central retinal area, while the number of cells of the inner nuclear layer was slightly reduced and that of the outer nuclear layer was still unchanged. The periphery of short duration diabetic retinae showed a normal cell content in all nuclear layers. In long-term diabetes (about 10 years), significant diminutions in cell numbers were found in all layers of both the retinal center and periphery. The described cell deficits are accounted for by disturbances of retinal microcirculation. After a relatively short duration of diabetes, blood flow interruptions in the area supplied by the central retinal artery occur; in long-term diabetics the chorioidal vessels are also affected. Connexions between the cell-deficit pattern and functional (electrophysiological) findings are discussed.
    Type of Medium: Electronic Resource
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  • 7
    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.
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  • 8
    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
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  • 9
    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
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  • 10
    ISSN: 1432-0568
    Keywords: Müller cells ; Radial glia ; Rabbit retina ; Cell processes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Radial glial (Müller) cells of the rabbit retina were studied by various techniques including Golgi impregnation, scanning electron microscopy, horseradish peroxidase application, and staining of enzymatically isolated cells. This combination of methods produced detailed information on the specialized morphology of the Müller cells within the different topographical regions of the retina, and of the Müller cell processes within the various retinal layers. As a general rule, the retinal periphery contains short thick Müller cells with big endfeet, whereas the thick central retina is occupied by long slender cells with small endfeet. Independent of their location within the retina, Müller cell processes were found to be adapted to the structure of the surrounding retinal layers. Within the outer and inner nuclear layers, Müller cell processes (and somata) extend thin cytoplasmic “bubbles” ensheathing the neuronal somata, as do the “velate” astrocytes in the brain. In the plexiform layers, Müller cells extend many fine side branches between the neuropil, comparable to the protoplasmic astrocytes of the brain. In the thick myelinated nerve fibre layer of the central retina the Müller cell processes are rather smooth, similar to those of fibrous astrocytes. It is concluded that the neuronal microenvironment determines the morphology of a given glial process, or even of a part of a glial process running through a specialized neuronal compartment.
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