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The Müller (Glial) Cell in Normal and Diseased Retina: A Case for Single-Cell ElectrophysiologyReichenbach A.a · Faude F.b · Enzmann V.b · Bringmann A.a · Pannicke T.a · Francke M.a · Biedermann B.a · Kuhrt H.a · Stolzenburg J.-U.a · Skatchkov S.N.d · Heinemann U.c · Wiedemann P.b · Reichelt W.a
aDepartment of Neurophysiology, Paul Flechsig Institute for Brain Research, and bDepartment of Ophthalmology, Leipzig University, Leipzig, and cDepartment of Neurophysiology, Institute of Physiology at the Charité, Medical Faculty of the Humboldt University, Berlin, Germany; dCenter for Molecular and Behavioral Neuroscience, Universidad Central del Caribe, Bayamon, P.R., USA
In the retina of most vertebrates there exists only one type of macroglia, the Müller cell. Müller cells express voltage-gated ion channels, neurotransmitter receptors and various uptake carrier systems. These properties enable the Müller cells to control the activity of retinal neurons by regulating the extracellular concentration of neuroactive substances such as K+, GABA and glutamate. We show here how electrophysiological recordings from enzymatically dissociated mammalian Müller cells can be used to study these mechanisms. Müller cells from various species have Na+-dependent GABA uptake carriers, but only cells from primates have additional GABA receptors that activate Cl–– channels. Application of glutamate analogues causes enhanced membrane currents recorded from Müller cells in situ but not from isolated cells. We show that mammalian Müller cells have no ionotropic glutamate receptors but respond to increased K+ release from glutamate-stimulated retinal neurons. This response is involved in extracellular K+ clearance and is mediated by voltagegated (inwardly rectifying) K+ channels which are abundantly expressed by healthy Müller cells. In various cases of human retinal pathology, currents through these channels are strongly reduced or even extinguished. Another type of voltagegated ion channels, observed in Müller cells from many mammalian species, are Na+ channels. In Müller cells from diseased human retinae, voltage-dependent Na+ currents were significantly increased in comparison to cells from control donors. Thus, the expression of glial ion channels seems to be controlled by neuronal signals. This interaction may be involved in the pathogenesis of retinal gliosis which inevitably accompanies any degeneration of retinal neurons. In particular, Müller cell proliferation may be triggered by mechanisms requiring the activation of Ca2+-dependent K+ channels. Ca2+-dependent K+ currents are easily elicitable in Müller cells from degenerating retinae and can be blocked by 1 mM TEA (tetraethylammonium). In purified Müller cell cultures, the application of 1 mM TEA greatly reduces the proliferative activity of the cells. These data clearly show that Müller cells are altered in cases of neuronal degeneration and may be crucially involved in pathogenetic mechanisms of the retina.
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