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Biomedical subjects

A Reichenbach

Publications and source records attributed to A Reichenbach.

At least 145 records · Page 8Linked to original sources
PubMed1988

Ultrastructure of rabbit retinal nerve fibre layer--neuro-glial relationships, myelination, and nerve fibre spectrum.

The ultrastructure of the rabbit retinal nerve fibre layer was studied both in retinal centre and periphery. The central nerve fibre layer was found to contain large masses of--mostly myelinated--nerve fibres, somata and processes of astrocytes and oligodendrocytes, vitreal processes of Müller cells, and blood vessels. Astrocyte and Müller cell processes could be discriminated both by their direction and by the thickness of their intermediate filaments which was about 7 nm in Müller cells and about 10 nm in astrocytes. Some peculiarities of nuclei and cytoplasmic organelles of rabbit retinal astrocytes and oligodendrocytes are described. Myelin sheaths are demonstrated to be derived from oligodendrocytes; in some cases, two axons were found within a common myelin sheath. In the retinal periphery, only sparse thin bundles of unmyelinated axons were found in between a thick row of big Müller cell endfeet; astrocytes, oligodendrocytes, and blood vessels were missing here. In both retinal regions, node-like membrane specializations of optic axons were found; these were always surrounded by a corona of fine glial processes arising from astrocytes as well as from Müller cells. The features of myelination within the rabbit nerve fibre layer were quantified, and compared with recent literature data. A hypothesis is offered relating the production of myelin to the release of diffusable substance(s) by active axons. This hypotheses allows to account for the striking finding that relatively thick axons remain unmyelinated in the nerve fibre layer of most mammalian retinae like in the rabbit retinal periphery whereas they become myelinated in the central rabbit retina like in central nervous system in general.

Animals↗
PubMed1987

High Na+ affinity of the Na+,K+ pump in isolated rabbit retinal Müller (glial) cells.

Rabbit retinal Müller (glial) cells were isolated by means of papain and mechanical dissociation. In a special perfusion chamber, the cells were penetrated with a recording microelectrode. Membrane potential changes were recorded in response to extracellular application of both high-K+ solutions and of ouabain, and that during perfusion with normal and Na+-free solutions, respectively. In other Müller cell preparations, Na+,K+-adenosine triphosphatase (ATPase) activity was measured using a radiochemical method, and its Na+ dependence was determined. All results strongly suggest that the Müller cell's Na+,K+ pump can be activated in the presence of extremely low amounts of Na+. This provides additional evidence for significant differences between the glial and the neuronal enzyme.

Animals↗
PubMed1987

Cell length to diameter relation of rat fetal radial glia--does impaired K+ transport capacity of long thin cells cause their perinatal transformation into multipolar astrocytes?

In thick sections of Golgi-impregnated late fetal rat brains, radial glial cells were measured for both length and diameter of their main (basal) processes. The process diameter was found to decrease proportionally to the square root of cell length; thus, the cytoplasm volume remained fairly constant for cells in the range of lengths studied (100-2500 microns). The measured data were used for calculation of the cell's space constant lambda in order to estimate their capability to carry spatial buffering K+ currents. These calculations show that long and slender cells are unable to perform sufficient K+ clearance by such currents. This supports the hypothesis that perinatally when the maturing neurons release enhanced K+ during electrical activity, such long thin cells are subject to long-lasting depolarizations and, thereby, forced to undergo mitotic cell division transforming them into multipolar astrocytes.

Animals↗
PubMed1987

Quantitative-morphometric aspects of Bergmann glial (Golgi epithelial) cell development in rats. A Golgi study.

Bergmann glial (Golgi epithelial) cells in the cerebella of rats of various ages were stained by the rapid Golgi technique, and their radial stem processes were measured for length and diameter. Additionally, the average number of such processes per cell was counted, and the development of bushy lateral protrusions was quantified. The length of radial processes--depending on the thickness of the molecular layer--was found to increase up to the end of the 2nd year of life. This elongation was accompanied by a reduction of the mean process diameter which was, however, not sufficient to prevent an increase in the cytoplasmic volume of the elongating cells. A marked outgrowth of lateral protrusions was observed up to at least the 5th month of life. These data are compared with earlier findings on the development of rat brain stem fetal radial glia, and of rabbit retinal Müller cells. Common mechanisms of glial cell development are discussed.

Age Factors↗
PubMed1987

Spatial buffering of potassium by retinal Müller (glial) cells of various morphologies calculated by a model.

In a previous study we found the morphometrical data of rabbit retinal Müller (radial glial) cells to vary greatly with their localization in various parts of the retina. The long cells of the central retina have thinner vitreal processes and smaller endfeet than the short cells of the retinal periphery. This configuration should impair the spatial buffering capacity of the central Müller cells for excess K+ ions. To test this hypothesis, we developed a simple modified model for the calculation of K+ clearance by spatial buffering, diffusion through the extracellular space, and co-operation of both processes. K+ clearance processes were demonstrated to depend greatly on the retinal geometry and Müller cell morphology in different parts of the retina. The efficiency of spatial buffering exhibited an obvious optimum for Müller cells of intermediate length, and decreased very steeply in longer cells. Some conclusions are drawn with respect to retinal physiology. In particular, it is suggested that very long and slender radial glia is unable to perform sufficient K+ clearance preventing long-lasting extracellular [K+] elevations after neuronal activity. Such [K+] elevations could depolarize these glial cells so as to enforce their mitotic division. This mechanism might lead to the perinatal transformation of embryonic radial glia into adult multipolar glia when neuronal activity commences in CNS tissues thicker than the maximal effective length of radial glial cells.

Animals↗
PubMed1987

Quantitative and qualitative morphology of rabbit retinal glia. A light microscopical study on cells both in situ and isolated by papaine.

Rabbit retinal glia was studied by light microscopy of both stained sections of frozen retinae and enzymatically isolated cells. In the vast majority of this tissue, except for a small region around the optic nerve head, the glia consists solely of radial glia, i.e. Müller cells whose morphology was found to depend markedly on their topographic localization within the retina. Müller cells in the periphery are short and have thick vitreal processes bearing a single large endfoot. Central Müller cells are long and slender; through the thickening nerve fibre layer they send vitreal processes which are subdivided into several fine branches ending with multiple small endfeet. Müller cells in the retinal centre are far more closely packed than those in the periphery; everywhere, however, a constant ratio of Müller cells: neurons of about 1:15 was found, except for the juxta-optic nerve head region where this ratio is slightly reduced. Where the central retina reaches a thickness requiring Müller cell lengths of more than 130 micron, additional non-radial glial cells occur within the nerve fibre layer. The majority of these cells seem to be astrocytes. Their number per retinal area increases with the thickening of both the whole retina and the nerve fibre layer. The occurrence of these non-radial glial cells leads to an enhancement of the glia:neuron index in the retinal centre. Possible mechanisms of physiological control of gliogenesis are discussed.

Animals↗
PubMed1986

Postnatal development of radial glial (Müller) cells of the rabbit retina.

Radial glial (Müller) cells were isolated from postnatal rabbit retinae by enzymatic dissociation in papain-containing solution, air-dried, and submitted to Pappenheim's panoptic stain. Morphometric data of these cells were evaluated by light microscopy. During postnatal development, the cells become substantially thicker and shorter, their nuclei lose the rod shape and move more toward scleral layers, and the nucleus-cytoplasm volume relation decreases. Whereas the cell volume increases from birth on, substantial outgrowth of fine side branches within the plexiform layers fails to occur before electrical activity is established there, i.e. after postnatal day 9. A model is proposed relating the growth of sheath-bearing glial processes to local protein synthesis stimulated by external K+ accumulation due to neuronal activity. Early myelinated nerve fibers are suggested to bear mechanical resistance to growing radial glial processes thus causing a splitting of these processes when they enter developing nerve fiber layers.

Animals↗
PubMed1986

Potassium accumulation by the glial membrane pump as revealed by membrane potential recording from isolated rabbit retinal Müller cells.

Müller (glial) cells were isolated from rabbit retinae by papaine and mechanical dissociation. In a special perfusion chamber, the cells were penetrated with a recording electrode. When high-K+ solutions were applied into the environment of the cells by means of a second micropipette, the cell membrane depolarized strongly. During prolonged application of high-K+ solutions, however, there occurred a marked repolarization, and after cessation of high-K+ application, a strong hyperpolarization was observed. Both effects disappeared under the influence of ouabain, suggesting the accumulation of intracellular K+ by an active membrane pump. The data were used for calculation of the membrane's Na+:K+ permeability ratio, the intracellular K+ concentration, the pump rate and the mean pump site density. The calculated values are in good agreement with published data from mammalian astrocytes and are compared with those from amphibian Müller cells.

Animals↗
PubMed1986

Intracellular recordings from isolated rabbit retinal Müller (glial) cells.

Müller (glial) cells were isolated from rabbit retinae by papaine and mechanical dissociation. The cells were fixed on a gelatine-covered glass slide by means of concanavalin A, and the slide was mounted in a perfusion chamber under a light microscope with modified optics. Besides the recording microelectrode, two other micropipettes could be adjusted with their tips near the cell. These micropipettes were used for application of test solutions into the environment of the cells. On application of high K+ solutions, the cell depolarized strongly but during prolonged application there was a marked repolarization. After the end of high K+ application the cells showed a hyperpolarization which was enhanced in both amplitude and duration with prolongation of the K+ exposure. Both repolarization and afterhyperpolarization disappeared under ouabain. Ouabain application itself caused a small reversible depolarization. Na+ free solution caused hyperpolarization. The results suggest the existence of an active membrane pump mechanism in our cells. This pump seems to be electrogenic under our experimental conditions and seems to be activated even in the absence of sodium. The cell membrane is demonstrated to contain a significant Na+ conductance.

Animals↗
PubMed1986

Morphometric parameters of Müller (glial) cells dependent on their topographic localization in the nonmyelinated part of the rabbit retina. A consideration of functional aspects of radial glia.

Morphometric parameters of Müller cells were evaluated by light microscopy both in whole retinae and in enzymatically isolated cells from adult pigmented rabbits. In spite of the marked decrease in cell densities from visual streak to far periphery, a constant glia-neuron ratio of about 1:15 was found in all regions. The volume of individual Müller cells was found to increase strongly when the cells become shorter, i.e. when the retinal centre was compared to the retinal periphery. The contribution of Müller cell volume to the total retinal volume, however, was shown to be constant at about 6%. Long Müller cells have a thin vitreal process and a small vitreal endfoot surface. The consequences of this rule for the proposed function of Müller cells in retinal K+ clearance are discussed with respect to general features of radial glia. It is suggested that foetal radial glial cells too long to perform sufficient K+ clearance are destined to be transformed into 'adult' multipolar glia by mitotic cell division.

Animals↗
PubMed1985

Na+,K+-activated adenosine triphosphatase of isolated Müller cells from the rabbit retina shows a K+ dependence similar to that of brain astrocytes.

Müller (glial) cells from the rabbit retina were isolated by means of papain and mechanical dissociation. Their Na+,K+-adenosine triphosphatase (ATPase) activity was measured using a radiochemical method, and its K+ dependence was determined. In contrast to that of photoreceptors (data from the literature), the Na+,K+-ATPase of Müller cells could be shown to increase its activity greatly when the [K+] was enhanced up to 10 mM. The functional implications of this behaviour for the K+ clearance in the retina are discussed.

Animals↗
PubMed1985

Retinitis-pigmentosa-like tapetoretinal degeneration in a rabbit breed.

By chance, we found a rabbit strain with retinal dystrophy. The eyes of these rabbits were examined by ophthalmoscopy, electroretinography, histology, and cytology--the latter after retina dissociation with papaine. The results suggest this rabbit strain to be a possible animal model for human retinitis pigmentosa.

Animals↗
PubMed1985

Effects of alpha-aminoadipic acid on the glutamate-isolated P III of the rabbit electroretinogram.

alpha-Aminoadipic acid was intravitreally applied to adult rabbits. After 5 h, the retinae of these animals were examined by electroretinography and histochemistry. The retinal Müller cells were extremely swollen, and the electroretinographic slow P III was extinguished. The mass receptor potential was somewhat diminished. The results are consistent with the opinion that the slow P III is the reaction of the Müller cells to the changed external potassium ion concentration caused by the activity of the photoreceptors.

2-Aminoadipic Acid↗
PubMed1985

Morphological variability, lectin binding and Na+,K+-activated adenosine triphosphatase activity of isolated Müller (glial) cells from the rabbit retina.

Rabbit retinal Müller cells were isolated by means of papaine and mechanical dissociation. These cells were shown to have a well preserved morphology and to preserve viability for many hours. Intense wheat germ agglutinin binding occurs on the photoreceptor side of Müller cells, especially in the microvillous region. Rabbit retinal Müller cells have a Na+,K+-activated adenosine triphosphatase activity in the same order of magnitude as brain astroglial cells.

Animals↗
PubMed1985

Morphometric analysis of retinal blood vessels in retinopathia diabetica.

A quantitative investigation of the retinal blood vessels was carried out in 80 diabetics and 20 metabolically healthy controls of the same age and sex distribution. The blood vessels were isolated by trypsinization, stained with PAS, and analyzed by light microscopy. After 1-5 years' duration of diabetes mellitus, capillary lesions in the ocular fundus can be seen microscopically in the slides, but not with a stereomicroscope. In the retinae of persons with normal carbohydrate metabolism, capillary defects were found to a far lesser extent; they were also always localized in the periphery of the retina, whereas the diabetic lesions were localized in the retinal center. In the diabetics, both capillary lesions (e.g., loss of pericytes) and damage of the retinal neurons occurred nearly simultaneously and with the same retinal localization. This suggests that the capillary lesions are not the cause of neuronal degeneration but that both events are caused by the same mechanisms of pathogenesis.

Adult↗