Feasibility of EXIME® temporary prosthesis placement and removal in men with acute or chronic urinary retention after failure or inability to selfcatheterize.

INTRODUCTION: Urological emergencies represent 7% of admissions, 29% of which are acute urine retention. We report the first results of a protocol evaluating a new device in case of failure of self-catheterization, replacing a permanent catheter: the urethral device EXIME®. METHOD: Intention-to-treat study on the feasibility of inserting the EXIME® prosthesis in a day hospital after simple urethral gel instillation in men with urine retention. EXIME® was proposed to all patients after failure of Foley catheter removal and refusal or inability to learn self-catheterization. The protocol was referenced (NCT04218942) after obtaining the agreement of the committee for the protection of individuals. RESULTS: Among 278 patients admitted for a trial of Foley catheter removal, 15 patients with failed voiding resumption and refusal or failure of self-catheterization were offered the prosthesis. The median age was 73 years with a median retention volume of 700mL. The median prostatic volume was 60g. Fourteen patients had their prosthesis inserted in good conditions of comfort for the practitioner and the patient. One failed placement was noted. The difficulty of insertion was estimated by the practitioner at 0 on median (VAS from 0 to 10), and for its removal at 0. The pain during the insertion of the device was evaluated by the patients at 2.00 and for the removal at 0 (VAS from 0 to 10). 6 patients had satisfactory voiding recovery at D0. DISCUSSION: We proposed the placement of EXIME to patients who had failed the trial of Foley removal and were unable and/or unwilling to self-catheterize. These were patients with poor bladder contractility and a high risk of retention recurrence. Despite this mixed result, the simplicity of the device and the comfortable expectation of an endoscopic procedure seem promising. CONCLUSION: Insertion and retrieval of EXIME®prostatic prosthesis were easy and well tolerated in our population. Insertion failed in one patient. A comparative prospective study with self catheterization is necessary to determine its effectiveness.

Effects of transcranial magnetic stimulation on visual evoked potentials in a visual suppression task.

Transcranial magnetic stimulation (TMS) can non-invasively modify cortical neural activity by means of a time-varying magnetic field. For example, in cognitive neuroscience, it is applied to create reversible "virtual lesions" in healthy humans (usually assessed as diminished performance in a behavioral task), thereby helping to establish causal structure-function relationships. Despite its widespread use, it is still rather unclear how TMS acts on existing, task-related neural activity, potentially resulting in a measurable effect on the behavioral level. Here, we deliver TMS to early visual areas while recording EEG in order to directly characterize the interaction between TMS-evoked (TEPs) and visual-evoked potentials (VEPs). Simultaneously, the subjects' performance is assessed in a visual forced-choice task. This allows us to compare the TMS effects on the VEPs across different levels of behavioral impairment. By systematically varying the stimulation intensity, we demonstrate that TMS strongly enhances the overall visual stimulus-related activity (rather than disrupting it). This enhancement effect saturates when behavior is impaired. This might indicate that the neural coding of the visual stimulus is robust to noise within a certain dynamic range (as indexed by the enhancement). Strong disturbances might saturate this range, causing behavioral impairment. Variation of the timing between the visual stimulus and the magnetic pulse reveals a "constructive interference" between the TEPs and VEPs: The better the overlap between both evoked potentials, the stronger the interaction effect when TMS and visual stimulation are combined. Importantly, however, this effect is uncorrelated with the strength of behavioral impairment.

The cortical site of visual suppression by transcranial magnetic stimulation.

In visual suppression paradigms, transcranial magnetic stimulation (TMS) applied approximately 90 ms after visual stimulus presentation over occipital visual areas can robustly interfere with visual perception, thereby most likely affecting feedback activity from higher areas (Amassian VE, Cracco RQ, Maccabee PJ, Cracco JB, Rudell A, Eberle L. 1989. Suppression of visual perception by magnetic coil stimulation of human occipital cortex. Electroencephalogr Clin Neurophysiol 74:458-462.). It is speculated that the observed effects might stem primarily from the disruption of V1 activity. This hypothesis, although under debate, argues in favor of a special role of V1 in visual awareness. In this study, we combine TMS, functional magnetic resonance imaging, and calculation of the induced electric field to study the neural correlates of visual suppression. For parafoveal visual stimulation in the lower right half of the visual field, area V2d is shown to be the likely TMS target based on its anatomical location close to the skull surface. Furthermore, isolated stimulation of area V3 also results in robust visual suppression. Notably, V3 stimulation does not directly affect the feedback from higher visual areas that is relayed mainly via V2 to V1. These findings support the view that intact activity patterns in several early visual areas (rather than merely in V1) are likewise important for the perception of the stimulus.

Glia: the fulcrum of brain diseases.

Neuroglia represented by astrocytes, oligodendrocytes and microglial cells provide for numerous vital functions. Glial cells shape the micro-architecture of the brain matter; they are involved in information transfer by virtue of numerous plasmalemmal receptors and channels; they receive synaptic inputs; they are able to release 'glio'transmitters and produce long-range information exchange; finally they act as pluripotent neural precursors and some of them can even act as stem cells, which provide for adult neurogenesis. Recent advances in gliology emphasised the role of glia in the progression and handling of the insults to the nervous system. The brain pathology, is, to a very great extent, a pathology of glia, which, when falling to function properly, determines the degree of neuronal death, the outcome and the scale of neurological deficit. Glial cells are central in providing for brain homeostasis. As a result glia appears as a brain warden, and as such it is intrinsically endowed with two opposite features: it protects the nervous tissue as long as it can, but it also can rapidly assume the guise of a natural killer, trying to eliminate and seal the damaged area, to save the whole at the expense of the part.

Microdomains for neuron-glia interaction: parallel fiber signaling to Bergmann glial cells.

Astrocytes are considered a reticulate network of cells, through which calcium signals can spread easily. In Bergmann glia, astrocytic cells of the cerebellum, we identified subcellular compartments termed 'glial microdomains'. These elements have a complex surface consisting of thin membrane sheets, contain few mitochondria and wrap around synapses. To test for neuronal interaction with these structures, we electrically stimulated parallel fibers. This stimulation increased intracellular calcium concentration ([Ca2+]i) in small compartments within Bergmann glial cell processes similar in size to glial microdomains. Thus, a Bergmann glial cell may consist of hundreds of independent compartments capable of autonomous interactions with the particular group of synapses that they ensheath.

The Müller cell: a functional element of the retina.

Müller cells are the principal glial cells of the retina, assuming many of the functions carried out by astrocytes, oligodendrocytes and ependymal cells in other CNS regions. Müller cells express numerous voltage-gated channels and neurotransmitter receptors, which recognize a variety of neuronal signals and trigger cell depolarization and intracellular Ca2+ waves. In turn, Müller cells modulate neuronal activity by regulating the extracellular concentration of neuroactive substances, including: (1) K+, which is transported via Müller-cell spatial-buffering currents; (2) glutamate and GABA, which are taken up by Müller-cell high-affinity carriers; and (3) H+, which is controlled by the action of Müller-cell Na(+)-HCO3- co-transport and carbonic anhydrase. The two-way communication between Müller cells and retinal neurons indicates that Müller cells play an active role in retinal function.

The pecten oculi of the chicken: a model system for vascular differentiation and barrier maturation.

The pecten oculi is a convolute of blood vessels in the vitreous body of the avian eye. This structure is well known for more than a century, but its functions are still a matter of controversies. One of these functions must be the formation of a blood-retina barrier because there is no diffusion barrier for blood-borne compounds available between the pecten and the retina. Surprisingly, the blood-retina barrier characteristics of this organ have not been studied so far, although the pecten oculi may constitute a fascinating model of vascular differentiation and barrier maturation: Pectinate endothelial cells grow by angiogenesis from the ophthalmotemporal artery into the pecten primordium and consecutively gain barrier properties. The pectinate pigmented cells arise during development from retinal pigment epithelial cells and subsequently lose barrier properties. These inverse transdifferentiation processes may be triggered by the peculiar microenvironment in the vitreous body. In addition, the question is discussed whether the avascularity of the avian retina may be due to the specific metabolic activity of the pecten.

Potassium as a signal for both proliferation and differentiation of rabbit retinal (Müller) glia growing in cell culture.

Retinal glial (Müller) cells were grown from explants of early postnatal rabbit retinae. The resulting monolayers of flat cells were exposed to control media (containing 5.85 mM K+), and to media with enhanced K+ concentrations (10 and 20 mM) or arginine-vasopressin (AVP, 20 micrograms/ml) or epithelial growth factor (EGF, 10 ng/ml). Autoradiographically, protein synthesis was quantified as L-[3H]-lysine incorporation, and DNA synthesis as [3H]-thymidine incorporation. Furthermore, the activity of Na+,K(+)-ATPase was measured radiochemically. Short exposure to either moderately enhanced K+ concentrations (10 mM) or to AVP, stimulated L-[3H]-lysine incorporation into the cells. Long-lasting exposure to either high K+ concentrations (20 mM) or to EGF stimulated [3H]-uptake. The Na+,K(+)-ATPase activity of cell cultures increased with increasing K+ concentration of the media. It is suggested that release of K+ by active neuronal compartments stimulates local protein synthesis of glial cells, resulting in the formation of glial sheaths with active K+ uptake capacity. Strong K+ release may even induce glial proliferation.

Brain-derived neurotrophic factor inhibits osmotic swelling of rat retinal glial (Müller) and bipolar cells by activation of basic fibroblast growth factor signaling.

Water accumulation in retinal glial (Müller) and neuronal cells resulting in cellular swelling contributes to the development of retinal edema and neurodegeneration. Intravitreal administration of neurotrophins such as brain-derived neurotrophic factor (BDNF) is known to promote survival of retinal neurons. Here, we show that exogenous BDNF inhibits the osmotic swelling of Müller cell somata induced by superfusion of rat retinal slices or freshly isolated cells with a hypoosmotic solution containing barium ions. BDNF also inhibited the osmotic swelling of bipolar cell somata in retinal slices, but failed to inhibit the osmotic soma swelling of freshly isolated bipolar cells. The inhibitory effect of BDNF on Müller cell swelling was mediated by activation of tropomyosin-related kinase B (TrkB) and transactivation of fibroblast growth factor receptors. Exogenous basic fibroblast growth factor (bFGF) fully inhibited the osmotic swelling of Müller cell somata while it partially inhibited the osmotic swelling of bipolar cell somata. Isolated Müller cells displayed immunoreactivity of truncated TrkB, but not full-length TrkB. Isolated rod bipolar cells displayed immunoreactivities of both TrkB isoforms. Data suggest that the neuroprotective effect of exogenous BDNF in the retina is in part mediated by prevention of the cytotoxic swelling of retinal glial and bipolar cells. While BDNF directly acts on Müller cells by activation of TrkB, BDNF indirectly acts on bipolar cells by inducing glial release of factors like bFGF that inhibit bipolar cell swelling.

Quantitative phylogenetic constancy of cerebellar Purkinje cell morphological complexity.

Golgi-stained material of cerebellar cortices from 17 species was examined by measuring the fractal dimensions of the borders of Purkinje cells, which is a quantitative, objective measure of morphological complexity. Nine species (from birds to man) were chosen for a comparison with ANOVA and no statistically significant differences were found in their fractal dimensions. In contrast, a wide range of differences was found in the membrane areas across species lines. The Sholl coefficient, a measure of branch formation and termination away from the soma, showed no consistent pattern for each cell. We interpret our results as indicating a constancy in morphological cellular complexity of Purkinje cells during late evolutionary time.

Development of the rabbit retina: II. Müller cells.

Müller (glial) cells of the rabbit retina were stained with antibodies against the intermediate filament protein vimentin in retinal wholemounts from various developmental stages. Both the density of stained profiles and the mean diameter of these profiles were measured, with the microscope focus in the inner plexiform layer of the retinae. Within this retinal layer, every Müller cell possesses one stout vitread process; thus counts of the stained profiles allow an estimation of their number. After postnatal day (P) 9, the total number of stained cells was slightly above 4 million per retina; for the adult rabbit retina, this agrees well with earlier data obtained by our group based on another method, as well as with published data from other groups. We suggest that after P 9, only Müller cells are stained, and this population is numerically stable. In contrast, neonatal retinae contained significantly more stained profiles. This indicates that either the total number of Müller cells is reduced by "physiological cell death" or that additional cells are stained neonatally. We discuss why we favour the second possibility. After P 9, two peculiarities occur in the Müller cell population: (1) their density decreases gradually, to a greater extent in the retinal periphery than in the center (i.e., in the "visual streak"), and (2) Müller cell diameters increase, again more in the periphery than in the center. We argue that differential retinal expansion leads to dispersion of the pre-existing cell population and allows for widening of the Müller cell processes. We conclude that Müller cells can be used postnatally in the rabbit retina as "landmarks" of expansion.

Development of A-type (axonless) horizontal cells in the rabbit retina.

The development of A-type horizontal cells (HC) was studied in the rabbit retina between embryonic day (E)24 and adulthood [the day of birth was called postnatal day (P)1 and corresponds to E31-32]. The cells were visualized by several methods 1) by immunolabeling with antibodies to neurofilament 70,000 (NF-70kD), 2) by immunolabeling with antibodies to a calcium binding protein (CaBP-28kD), 3) by two different methods of silver impregnation, and 4) by histochemical demonstration of NADH-diaphorase activity. Most methods labeled A-type HC only in the dorsal retina; thus, our study is restricted to HC of this region. HC densities were determined at each developmental stage. The cells were drawn at scale, and size, quotient of symmetry, and topographical orientation of dendritic trees were studied by image analysis. The growth of HC dendritic fields was correlated with data on the postnatal local retinal expansion, which is known to be driven by the intraocular pressure (after cessation of retinal cell proliferation at P9). This expansion was evaluated in an earlier paper (Reichenbach et al. [1993] Vis. Neurosci. 10:479-498) by using local subpopulations of Müller cells as "markers" of distinct topographic regions of the retinae. After E24, when the final number of HC is established, we can discriminate three distinct developmental stages of A-type HC. During the first stage, between E24 and E27, the young cells are often vertically oriented and may extend their first short dendrites within (the primordia of) both plexiform layers. The irregular HC mosaic at E24 shows a significant difference to all other stages. The second stage begins after birth when the dendritic trees of the cells are already restricted to the outer plexiform layer. Between P3 and P9, their dendritic trees enlarge more than the surrounding retinal tissue expands, and the coverage factor almost doubles from 2.5 to 4.4. The third stage occurs after P9 when the growth rate of dendritic tree areas corresponds to that of the local retinal tissue expansion caused by "passive stretching" of the postmitotic tissue, and the coverage factor remains constant. This is compatible with the view that mature synaptic connections of A-type HC are mostly established after the first week of life and are then maintained.

Müller glial cells of the tree shrew retina.

The tree shrew is one of the few mammalian species whose retinae are strongly cone dominated, which is usually the case in reptilian and avian retinae. Müller cells of the tree shrew (Tupaia belangeri) retina were studied by transmission electron microscopy of tissue sections and freeze-fracture replicas, by immunolabeling of the intermediate filament protein vimentin in radial paraffin sections and in whole retinae, as well as by intracellular dye injection in slices of retinae. In addition, enzymatically isolated cells were stained by Pappenheim's panoptic staining method. The cells showed an ultrastructure that is similar to other mammalian Müller cells with two exceptions: Due to the extensive lateral fins of cone inner segments, the apical microvilli of Müller cells are arranged in peculiar palisades, and the basket-like Müller cell sheaths around neuronal somata in both nuclear layers consist of unusual multilayered membrane lamellae. Unlike Müller cells in other mammalian species studied thus far, but similar to reptilian and avian Müller cells, those of tree shrews commonly have two or more vitread processes rather than one main trunk. Müller cell densities range between some 13,000 mm-2 in the periphery and about 20,000 mm-2 in the retinal center. Neuron:(Müller)glial cell ratios were estimated to be 7.9:1 in the center and 6.2:1 in the periphery. For each Müller cell, about 1.5 (cone) photoreceptor cells, four or five interneurons of the inner nuclear layer, and about one cell of the ganglion cell layer were counted. This is a much lower number of neurons per Müller cell than in most other mammals studied.

Role of Muller cells in retinal degenerations.

Muller (radial glial) cells span the entire thickness of the retina, and contact and ensheath every type of neuronal cell body and process. This morphological relationship is reflected by a multitude of functional interactions between retinal neurons and Muller cells, including extracellular ion homeostasis and glutamate recycling by Muller cells. Virtually every disease of the retina is associated with a reactive Muller cell gliosis. Muller cell gliosis may either support the survival of retinal neurons or accelerate the progress of neuronal degeneration. Muller cells are key mediators of nerve cell protection, especially via release of basic fibroblast growth factor, via uptake and degradation of the excitotoxin glutamate, and via secretion of the antioxidant glutathione. Neovascularization during hypoxic conditions is mediated by Muller cells via release of vascular endothelial growth factor and transforming growth factor beta or via direct contact to endothelial cells. Primary Muller cell insufficiency has been suggested to be the cause of different cases of retinal degeneration including hepatic and methanol-induced retinopathy and glaucoma. It is conceivable that, in the future, new therapeutic strategies may utilize Muller cells for, e.g., somatic gene therapy or transdifferentiation of retinal neurons from dedifferentiated Muller cells.

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.

Alterations of potassium channel activity in retinal Müller glial cells induced by arachidonic acid.

Arachidonic acid, which is thought to be involved in pathogenetic mechanisms of the central nervous system, has been shown previously to modulate neuronal ion channels and the glutamate uptake carrier of retinal glial (Müller) cells. We have used various configurations of the patch-clamp technique to determine the effects of arachidonic acid on the K+ currents of freshly isolated Müller glial cells from rabbit and human. Arachidonic acid reduced the peak amplitude of the transient (A-type) outward K+ currents in a dose-dependent and reversible manner, with a 50% reduction achieved by 4.1 microM arachidonic acid. The inward rectifier-mediated currents remained unchanged after arachidonic acid application. The amplitude of the Ca(2+)-activated K+ outward currents (KCa), which were blocked by 1 mM tetraethylammonium chloride and 40 nM iberiotoxin, respectively, was dose-dependently elevated by bath application of arachidonic acid. The activation curve of the KCa currents shifted towards more negative membrane potentials. Furthermore, arachidonic acid was found to suppress inwardly directed Na+ currents. In cell-attached recordings with 3 mM K+ in the bath and 130 mM K+ in the pipette, the KCa channels of rabbit Müller cells displayed a linear current-voltage relation, with a mean slope conductance of 102 pS. In excised patches, the slope conductance was 220 pS (150 mM K+i/130 mM K+o). The opening probability of the KCa channels increased during membrane depolarization and during elevation of the free Ca2+ concentration at the intracellular face of the membrane patches. Bath application of arachidonic acid caused a reversible increase of the single-channel opening probability, as well as an increase of the number of open channels. Arachidonic acid did not affect the single-channel conductance. Since arachidonic acid also stimulates the KCa channel activity in excised patches, the action of arachidonic acid is assumed to be independent of changes of the intracellular calcium concentration. Our results demonstrate that arachidonic acid exerts specific effects on distinct types of K+ channels in retinal glial, cells. In pathological cases, elevated arachidonic acid levels may contribute to prolonged Müller cell depolarizations, and to the initiation of reactive glial cell proliferation.

P2 receptors in satellite glial cells in trigeminal ganglia of mice.

There is strong evidence for the presence of nucleotide (P2) receptors in sensory neurons, which might play a role in the transmission of pain signals. In contrast, virtually nothing is known about P2 receptors in satellite glial cells (SGCs), which are the main glial cells in sensory ganglia. We investigated the possibility that P2 receptors exist in SGCs in murine trigeminal ganglia, using Ca(2+) imaging, patch-clamp recordings, and immunohistochemistry. We found that ATP caused an increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in SGCs. As adenosine had no effect on [Ca(2+)](i), and the P2 receptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid largely blocked the response to ATP we conclude that P1 receptors did not contribute to the responses. We obtained the following evidence that the responses to ATP were mediated by metabotropic P2Y receptors: (i) persistence of the responses in Ca(2+)-free solution, (ii) inhibition of the response by cyclopiazonic acid, (iii) [Ca(2+)](i) increases in response to the P2Y agonists uridine triphosphate, adenosine thiodiphosphate, and 2-methylthio ADP, and (iv) failure of the P2X agonist alpha,beta-methylene ATP to elicit a response. Agonists of P2Y(1) receptors and uridine triphosphate, an agonist at P2Y(2) and P2Y(4) receptors, induced [Ca(2+)](i) increases suggesting that at least these P2Y receptor subtypes are present on SGCs. Using an antibody against the P2Y(4) receptor, we found immunopositive SGCs. Patch-clamp recordings of SGCs did not reveal any inward current due to ATP. Therefore, there was no evidence for the activation of ionotropic P2X receptors under the present conditions. The results indicate the presence of functional nucleotide (P2Y) receptors in SGCs.

Failure of potassium siphoning by Müller cells: a new hypothesis of perfluorocarbon liquid-induced retinopathy.

PURPOSE: To determine the effect of perfluorocarbon liquid (PFCL)-induced abolition of potassium siphoning by the vitreal end feet of Miller cells. METHODS: Porcine eyecups were filled with stained balanced salt solution and PFCLs (perfluorodecalin, perfluorooctane, perfluoroperhydrophenanthrene or the semifluorocarbon perfluorohexylhexane). With optical coherence tomography, the distance between PFCL and retina was determined, and the size of the aqueous space covering the retinal surface was estimated. The data were used to calculate the retinal potassium siphoning into small aqueous volumes. RESULTS: The distance between PFCL and retinal surface was found to be less than 5 to 10 microm with any PFCL tested. The resultant volume of the aqueous space was too small to act as a sufficient sink for K+ ion siphoning. CONCLUSIONS: A certain threshold volume of vitreal fluid seems to be necessary for efficient buffering of intraretinal increases of K+ and perhaps other (e.g., H+) ions through the Müller cells. When the aqueous fluid is replaced by a PFCL (or by silicone oil) for longer periods, the outer retina becomes subject to long-lasting K+ accumulation, and consequent neurodegeneration and reactive gliosis occurs. The authors propose to search for new vitreous-substituting fluids with the capability to dissolve ions.

Electrophysiology of rabbit Müller (glial) cells in experimental retinal detachment and PVR.

PURPOSE: To determine the electrophysiological properties of Müller (glial) cells from experimentally detached rabbit retinas. METHODS: A stable local retinal detachment was induced by subretinal injection of a sodium hyaluronate solution. Müller cells were acutely dissociated and studied by the whole-cell voltage-clamp technique. RESULTS: The cell membranes of Müller cells from normal retinas were dominated by a large inwardly rectifying potassium ion (K+) conductance that caused a low-input resistance (<100 M(Omega)) and a high resting membrane potential (-82 +/- 6 mV). During the first week after detachment, the Müller cells became reactive as shown by glial fibrillary acidic protein (GFAP) immunoreactivity, and their inward currents were markedly reduced, accompanied by an increased input resistance (>200 M(Omega)). After 3 weeks of detachment, the input resistance increased further (>300 M(Omega)), and some cells displayed significantly depolarized membrane potentials (mean -69 +/- 18 mV). When PVR developed (in 20% of the cases) the inward K+ currents were virtually completely eliminated. The input resistance increased dramatically (>1000 MOmega), and almost all cells displayed strongly depolarized membrane potentials (-44 +/- 16 mV). CONCLUSIONS: Reactive Müller cells are characterized by a severe reduction of their K+ inward conductance, accompanied by depolarized membrane potentials. These changes must impair physiological glial functions, such as neurotransmitter recycling and K+ ion clearance. Furthermore, the open probability of certain types of voltage-dependent ion channels (e.g., Ca2+-dependent K+ maxi channels) increases that may be a precondition for Müller cell proliferation, particularly in PVR when a dramatic downregulation of both inward current density and resting membrane potential occurs.

Facilitation of artificial retinal detachment for macular translocation surgery tested in rabbit.

PURPOSE: For macular translocation surgery, the native attached retina has to be detached either locally or completely. Although different surgical techniques are used, there is a general search for supporting procedures that facilitate and accelerate the retinal detachment. METHODS: Pars plana vitrectomies were performed in pigmented rabbits. In all experimental groups, a local retinal detachment was created by infusing the test solution with a thin glass micropipette attached to a glass syringe. In control animals a standard balanced salt solution was used at room temperature, in combination with a standard vitrectomy light source. In two test groups, a calcium- and magnesium-free solution was used for the vitrectomy, under illumination by a standard light source in group I (solution at room temperature) and group II (solution heated up to body temperature). In group III the rabbits were dark-adapted for half an hour, and then, during surgery, a red filter was used in front of the light source (standard balanced salt solution at room temperature). After the rabbits were killed at the end of surgery, the adherence of the retinal pigment epithelium (RPE) to the neural retina in the detachment area was quantified microscopically, and the morphologic integrity of the detached retinal tissue was examined by light and electron microscopy. No electrophysiology was performed. RESULTS: In all four groups, it was possible to detach the retina. The maximum adherence of the RPE cells to the neural retina was observed in the control group. Virtually no decrease in adherence was found in test group II (36 degrees C solution without calcium and magnesium), whereas a significant decrease was seen in both group I (calcium- and magnesium-free solution at room temperature) and group III (dark adaptation-red light technique; standard balanced salt solution at room temperature). In none of the experimental groups was any obvious damage of the retinal structure observed, even after exposure to the test solutions for 60 minutes. CONCLUSIONS: Both dark adaptation (red illumination) and the use of a calcium chloride- and magnesium chloride-free solution (at room temperature) can facilitate retinal detachment in macular translocation surgery. Both techniques are proposed as a gentle support for the operation, because they protect an intact RPE cell layer and do not cause retinal damage at the ultrastructural level.