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Dive into the research topics where Thomas Pannicke is active.

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Featured researches published by Thomas Pannicke.


Journal of Neurochemistry | 2012

Glial cells in (patho)physiology.

Vladimir Parpura; Michael T. Heneka; Vedrana Montana; Stéphane H. R. Oliet; Arne Schousboe; Philip G. Haydon; Randy F. Stout; David C. Spray; Andreas Reichenbach; Thomas Pannicke; Milos Pekny; Marcela Pekna; Robert Zorec; Alexei Verkhratsky

J. Neurochem. (2012) 121, 4–27.


Progress in Retinal and Eye Research | 2009

Cellular signaling and factors involved in Müller cell gliosis: Neuroprotective and detrimental effects

Andreas Bringmann; Ianors Iandiev; Thomas Pannicke; Antje Wurm; Margrit Hollborn; Peter Wiedemann; Neville N. Osborne; Andreas Reichenbach

Müller cells are active players in normal retinal function and in virtually all forms of retinal injury and disease. Reactive Müller cells protect the tissue from further damage and preserve tissue function by the release of antioxidants and neurotrophic factors, and may contribute to retinal regeneration by the generation of neural progenitor/stem cells. However, Müller cell gliosis can also contribute to neurodegeneration and impedes regenerative processes in the retinal tissue by the formation of glial scars. This article provides an overview of the neuroprotective and detrimental effects of Müller cell gliosis, with accounts on the cellular signal transduction mechanisms and factors which are implicated in Müller cell-mediated neuroprotection, immunomodulation, regulation of Müller cell proliferation, upregulation of intermediate filaments, glial scar formation, and the generation of neural progenitor/stem cells. A proper understanding of the signaling mechanisms implicated in gliotic alterations of Müller cells is essential for the development of efficient therapeutic strategies that increase the supportive/protective and decrease the destructive roles of gliosis.


Molecular and Cellular Neuroscience | 2004

A potassium channel-linked mechanism of glial cell swelling in the postischemic retina.

Thomas Pannicke; Ianors Iandiev; Ortrud Uckermann; Bernd Biedermann; Franziska Kutzera; Peter Wiedemann; Hartwig Wolburg; Andreas Reichenbach; Andreas Bringmann

The cellular mechanisms underlying glial cell swelling, a central cause of edema formation in the brain and retina, are not yet known. Here, we show that glial cells in the postischemic rat retina, but not in control retina, swell upon hypotonic stress. Swelling of control cells could be evoked when their K(+) channels were blocked. After transient ischemia, glial cells strongly downregulated their K(+) conductance and their prominent Kir4.1 protein expression at blood vessels and the vitreous body. In contrast, the expression of the aquaporin-4 (AQP4) (water channel) protein was only slightly altered after ischemia. Activation of D(2) dopaminergic receptors prevents the hypotonic glial cell swelling. The present results elucidate the coupling of transmembraneous water fluxes to K(+) currents in glial cells and reveal the role of altered K(+) channel expression in the development of cytotoxic edema. We propose a mechanism of postischemic glial cell swelling where a downregulation of their K(+) conductance prevents the emission of intracellularly accumulated K(+) ions, resulting in osmotically driven water fluxes from the blood into the glial cells via aquaporins. Inhibition of these water fluxes may be beneficial to prevent ischemia-evoked glial cell swelling.


Neurochemistry International | 2009

Role of retinal glial cells in neurotransmitter uptake and metabolism

Andreas Bringmann; Thomas Pannicke; Bernd Biedermann; Mike Francke; Ianors Iandiev; Jens Grosche; Peter Wiedemann; Jan Albrecht; Andreas Reichenbach

In addition to photoreceptors and neurons, glial cells (in particular Müller cells) contribute to the removal and metabolization of neurotransmitters in the neural retina. This review summarizes the present knowledge regarding the role of retinal glial cells in the uptake of glutamate, N-acetylaspartylglutamate, gamma-aminobutyric acid, glycine, and d-serine, as well as the degradation and removal of purinergic receptor agonists. Some major pathways of glutamate metabolism in Müller cells are described; these pathways are involved in the glutamate-glutamine cycle of the retina, in the defense against oxidative and nitrosative stress via the production of glutathione, and in the production of substrates for the neuronal energy metabolism. In addition, the developmental regulation of the major glial glutamate transporter, GLAST, and of the glia-specific enzyme glutamine synthetase is described, as well as the importance of a malfunction and even reversal of glial glutamate transporters, and a downregulation of the glutamine synthetase, as pathogenic factors in different retinopathies.


Graefes Archive for Clinical and Experimental Ophthalmology | 2007

Müller cells as players in retinal degeneration and edema

Andreas Reichenbach; Antje Wurm; Thomas Pannicke; Ianors Iandiev; Peter Wiedemann; Andreas Bringmann

BackgroundUnder normal conditions, Müller cells support neuronal activity and the integrity of the blood-retinal barrier, whereas gliotic alterations of Müller cells under pathological conditions may contribute to retinal degeneration and edema formation. A major function of Müller cells is the fluid absorption from the retinal tissue, which is mediated by transcellular water transport coupled to currents through potassium channels.MethodsAlterations of retinal Müller cells under pathological conditions were investigated by immunohistochemistry and recording their behavior under osmotic stress.ResultsIn animal models of various retinopathies, e.g., retinal ischemia, ocular inflammation, retinal detachment, and diabetes, it was found that Müller cells decrease the expression of their major potassium channel (Kir4.1). This alteration is associated with an impairment of the rapid water transport across Müller cell membranes, as recognizable in the induction of cellular swelling under hypoosmolar conditions. Osmotic swelling of Müller cells is also induced by oxidative stress and by inflammatory mediators such as arachidonic acid and prostaglandins.ConclusionsThe data suggest that a disturbed fluid transport through Müller cells is (in addition to vascular leakage) a pathogenic factor contributing to the development of retinal edema. Pharmacological re-activation of the retinal water clearance by Müller cells may represent an approach to the development of new edema-resolving drugs. Triamcinolone acetonide, which is clinically used to resolve edema, prevents osmotic swelling of Müller cells as it induces the release of endogenous adenosine and subsequent A1 receptor activation which results in the opening of ion channels. Apparently, triamcinolone resolves edema by both inhibition of vascular leakage and stimulation of retinal fluid clearance by Müller cells.


Glia | 2000

Role of glial K(+) channels in ontogeny and gliosis: a hypothesis based upon studies on Müller cells.

Andreas Bringmann; Mike Francke; Thomas Pannicke; Bernd Biedermann; Hannes Kodal; Frank Faude; Winfried Reichelt; Andreas Reichenbach

The electrophysiological properties of Müller cells, the principal glial cells of the retina, are determined by several types of K+ conductances. Both the absolute and the relative activities of the individual types of K+ channels undergo important changes in the course of ontogenetic development and during gliosis. Although immature Müller cells express inwardly rectifying K+ (KIR) currents at a very low density, the membrane of normal mature Müller cells is predominated by the KIR conductance. The KIR channels mediate spatial buffering K+ currents and maintain a stable hyperpolarized membrane potential necessary for various glial‐neuronal interactions. During “conservative” (i.e., non‐proliferative) reactive gliosis, the KIR conductance of Müller cells is moderately reduced and the cell membrane is slightly depolarized; however, when gliotic Müller cells become proliferative, their KIR conductances are dramatically down‐regulated; this is accompanied by an increased activity of Ca2+‐activated K+ channels and by a conspicuous unstability of their membrane potential. The resultant variations of the membrane potential may increase the activity of depolarization‐activated K+, Na+ and Ca2+ channels. It is concluded that in respect to their K+ current pattern, mature Müller cells pass through a process of dedifferentiation before proliferative activity is initiated. GLIA 29:35–44, 2000.


The FASEB Journal | 2011

Reactive glial cells: increased stiffness correlates with increased intermediate filament expression

Yun-Bi Lu; Ianors Iandiev; Margrit Hollborn; Nicole Körber; Elke Ulbricht; Petra G. Hirrlinger; Thomas Pannicke; Er-Qing Wei; Andreas Bringmann; Hartwig Wolburg; Ulrika Wilhelmsson; Milos Pekny; Peter Wiedemann; Andreas Reichenbach; Josef A. Käs

Increased stiffness of reactive glial cells may impede neurite growth and contribute to the poor regenerative capabilities of the mammalian central nervous system. We induced reactive gliosis in rodent retina by ischemia‐reperfusion and assessed intermediate filament (IF) expression and the viscoelastic properties of dissociated single glial cells in wild‐type mice, mice lacking glial fibrillary acidic protein and vimentin (GFAP−/−Vim−/−) in which glial cells are consequently devoid of IFs, and normal Long‐Evans rats. In response to ischemia‐reperfusion, glial cells stiffened significantly in wild‐type mice and rats but were unchanged in GFAP−/− Vim−/− mice. Cell stiffness (elastic modulus) correlated with the density of IFs. These results support the hypothesis that rigid glial scars impair nerve regeneration and that IFs are important determinants of cellular viscoelasticity in reactive glia. Thus, therapeutic suppression of IF up‐regulation in reactive glial cells may facilitate neuroregeneration.—Lu, Y.‐B., Iandiev, I., Hollborn, M., Korber, N., Ulbricht, E., Hirrlinger, P. G., Pannicke, T., Wei, E.‐Q., Bringmann, A., Wol‐burg, H., Wilhelmsson, U., Pekny, M., Wiedemann, P., Reichenbach, A., Kas, J. A. Reactive glial cells: increased stiffness correlates with increased intermediate filament expression. FASEB J. 25, 624–631 (2011). www.fasebj.org


Pain | 2004

The effects of axotomy on neurons and satellite glial cells in mouse trigeminal ganglion

Pavel S. Cherkas; Tian-Ying Huang; Thomas Pannicke; Michael Tal; Andreas Reichenbach; Menachem Hanani

&NA; Damage to peripheral nerves induces ectopic firing in sensory neurons, which can contribute to neuropathic pain. As most of the information on this topic is on dorsal root ganglia we decided to examine the influence of infra‐orbital nerve section on cells of murine trigeminal ganglia. We characterized the electrophysiological properties of neurons with intracellular electrodes. Changes in the coupling of satellite glial cells (SGCs) were monitored by intracelluar injection of the fluorescent dye Lucifer yellow. Electrophysiology of SGCs was studied with the patch‐clamp technique. Six to eight days after axotomy, the percentage of neurons that fire spontaneously increased from 1.6 to 12.8%, the membrane depolarized from −51.1 to −45.5 mV, the percentage of cells with spontaneous potential oscillations increased from 19 to 37%, the membrane input resistance decreased from 44.4 to 39.5 M&OHgr;, and the threshold for firing an action potential decreased from 0.61 to 0.42 nA. These changes are consistent with increased neuronal excitability. SGCs were mutually coupled around a given neuron in 21% of the cases, and to SGCs around neighboring neurons in only 4.8% of the cases. After axotomy these values increased to 37.1 and 25.8%, respectively. After axotomy the membrane resistance of SGCs decreased from 101 M&OHgr; in controls to 40 M&OHgr;, possibly due to increased coupling among these cells. We conclude that axotomy affects both neurons and SGCs in the trigeminal ganglion. The increased neuronal excitability and ectopic firing may play a major role in neuropathic pain.


Glia | 1997

Loss of inwardly rectifying potassium currents by human retinal glial cells in diseases of the eye

Mike Francke; Thomas Pannicke; Bernd Biedermann; Frank Faude; Peter Wiedemann; Andreas Reichenbach; Winfried Reichelt

We compared the inward K+ currents of Müller glial cells from healthy and pathologically changed human retinas. To this purpose, the whole‐cell voltage‐clamp technique was performed on noncultured Müller cells acutely isolated from human retinas. Cells originated from retinas of four healthy organ donors and of 24 patients suffering from different vitreoretinal and chorioretinal diseases. Müller cells from organ donors displayed inward K+ currents in the whole‐cell mode similar to those found in other species. In contrast, this pattern was clearly changed in the Müller cells from patient retinas. In whole‐cell recordings many Müller cells had strongly decreased inward K+ current amplitudes or lost these currents completely. Thus, the mean input resistance of Müller cells from patients was significantly increased to 1,129 ± 812 MΩ, compared to 279 ± 174 MΩ in Müller cells from healthy organ donor retinas. Accordingly, since the membrane potential is mainly determined by the K+ inward conductance in healthy Müller cells, a large amount of Müller cells from patient retinas had a membrane potential which was significantly lower than that of Müller cells from control eyes. The mean membrane potentials were −37 ± 24 mV and −63 ± 25 mV for patient and donor Müller cells, respectively. The newly described membrane characteristic changes of Müller cells from patient eyes are assumed to interfere severely with normal retinal function: (1) the retinal K+ homeostasis, which is partly regulated by the Müller cell‐mediated spatial buffering, should be disturbed, and (2) the diminished membrane potential should influence voltage‐dependent transporter systems of the Müller cells, e.g., the Na+‐dependent glutamate uptake. GLIA 20:210–218, 1997.


Neuroscience | 1997

The glutathione level of retinal Müller glial cells is dependent on the high-affinity sodium-dependent uptake of glutamate

Winfried Reichelt; J Stabel-Burow; Thomas Pannicke; H Weichert; Uwe Heinemann

The dependence of intracellular glutathione, an important radical scavenger, on the extracellular glutamate and cystine concentration and the velocity of the high affinity sodium/glutamate transporter was studied in freshly-isolated Müller glial cells of the guinea-pig, kept in vitro for up to 11 h. To this end the relative Müller cell glutathione levels were measured using the fluorescent dye monochlorobimane, using different concentrations of glutamate and cystine in Ringer solution. In some experiments L-buthionine-[S,R]-sulfoximine, a blocker of glutathione synthesis, or L-trans-pyrrolidine-2,4-dicarboxylic acid and L-alpha-aminoadipic acid, inhibitors of glutamate uptake, were added. The Müller cells maintained about 80% of the normal glutathione level when maintained in Ringer solution containing 100 microM glutamate for 11 h. When under these conditions 100 microM cystine was added, the glutathione level increased to values, which were even higher than those at the beginning of the incubation period. Addition of cystine without glutamate caused a run down of the glutathione level to about 45% of the normal level, which is comparable to the run down in pure Ringer solution. Likewise, application of L-buthionine-[S,R]-sulfoximine (5 mM) lead to a strong run down of the glutathione level even in glutamate/cystine (100 microM)-containing solution. A similar suppressing effect was observed using L-trans-pyrrolidine-2,4-dicarboxylic acid and L-alpha-aminoadipic acid in the presence of 100 microM cystine and glutamate. We conclude that the intracellular glutamate concentration of the Müller cells is determined by the extracellular glutamate concentration and the velocity of the sodium/glutamate uptake. Consequently, cystine uptake into Müller cells, which is performed by the cystine/glutamate antiporter, is fueled by the sodium/glutamate transporter with intracellular glutamate. Both glutamate and cystine are also substrates for glutathione synthesis. The glutathione level is logically limited by the capacity of the sodium/glutamate transporter to provide glutamate intracellularly for, first, cystine uptake and, second, direct insertion into glutathione. Accordingly, the glutathione level is reduced when the sodium/glutamate transporter is blocked. Thus, a diminution of the glutathione level should be taken into consideration when the effects of sodium/glutamate uptake failure and reduced intracellular glutamate concentrations are discussed.

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Antje Grosche

University of Regensburg

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