Müller cells, the principal glial cells of the vertebrate retina, are fundamental for the maintenance and function of neuronal cells. In most vertebrates, including humans, Müller cells abundantly express Kir4.1 inwardly rectifying potassium channels responsible for hyperpolarized membrane potential and for various vital functions such as potassium buffering and glutamate clearance; inter-species differences in Kir4.1 expression were, however, observed. Localization and function of potassium channels in Müller cells from the retina of crocodiles remain, hitherto, unknown.
We studied retinae of the Spectacled caiman (Caiman crocodilus fuscus), endowed with both diurnal and nocturnal vision, by (i) immunohistochemistry, (ii) whole-cell voltage-clamp, and (iii) fluorescent dye tracing to investigate K+ channel distribution and glia-to-neuron communications.
Immunohistochemistry revealed that caiman Müller cells, similarly to other vertebrates, express vimentin, GFAP, S100β, and glutamine synthetase. In contrast, Kir4.1 channel protein was not found in Müller cells but was localized in photoreceptor cells. Instead, 2P-domain TASK-1 channels were expressed in Müller cells. Electrophysiological properties of enzymatically dissociated Müller cells without photoreceptors and isolated Müller cells with adhering photoreceptors were significantly different. This suggests ion coupling between Müller cells and photoreceptors in the caiman retina. Sulforhodamine-B injected into cones permeated to adhering Müller cells thus revealing a uni-directional dye coupling.
Our data indicate that caiman Müller glial cells are unique among vertebrates studied so far by predominantly expressing TASK-1 rather than Kir4.1 K+ channels and by bi-directional ion and uni-directional dye coupling to photoreceptor cells. This coupling may play an important role in specific glia-neuron signaling pathways and in a new type of K+ buffering.
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"In the early 1990s, the existence of a glial subtype showing the same electrophysiological characteristic was confirmed by two pioneer patch-clamp studies from white matter and gray matter, and these glial cells were termed " passive astrocytes " (Berger et al. 1991; Steinhauser et al. 1992). Since then, passive conductance has been emerging as a general feature of astrocytes from low to high species, including humans (Han et al. 2013; Schroder et al. 2000; Zayas-Santiago et al. 2014). In the hippocampus, the passive astrocyte becomes the only electrophysiological phenotype after the third postnatal week; therefore, the loss of rectifying channel conductances appears to be an indication of functional maturation of astrocytes (Kafitz et al. 2008; Zhou et al. 2006). "
[Show abstract][Hide abstract] ABSTRACT: Gliosis of retinal Müller glial cells may have both beneficial and detrimental effects on neurons. To investigate the role of purinergic signaling in ischemia-induced reactive gliosis, transient retinal ischemia was evoked by elevation of the intraocular pressure in wild-type (Wt) mice and in mice deficient in the glia-specific nucleotide receptor P2Y1 (P2Y1 receptor-deficient (P2Y1R-KO)). While control retinae of P2Y1R-KO mice displayed reduced cell numbers in the ganglion cell and inner nuclear layers, ischemia induced apoptotic death of cells in all retinal layers in both, Wt and P2Y1R-KO mice, but the damage especially on photoreceptors was more pronounced in retinae of P2Y1R-KO mice. In contrast, gene expression profiling and histological data suggest an increased survival of amacrine cells in the postischemic retina of P2Y1R-KO mice. Interestingly, measuring the ischemia-induced downregulation of inwardly rectifying potassium channel (Kir)-mediated K(+) currents as an indicator, reactive Müller cell gliosis was found to be weaker in P2Y1R-KO (current amplitude decreased by 18%) than in Wt mice (decrease by 68%). The inner retina harbors those neurons generating action potentials, which strongly rely on an intact ion homeostasis. This may explain why especially these cells appear to benefit from the preserved Kir4.1 expression in Müller cells, which should allow them to keep up their function in the context of spatial buffering of potassium. Especially under ischemic conditions, maintenance of this Müller cell function may dampen cytotoxic neuronal hyperexcitation and subsequent neuronal cell loss. In sum, we found that purinergic signaling modulates the gliotic activation pattern of Müller glia and lack of P2Y1 has janus-faced effects. In the end, the differential effects of a disrupted P2Y1 signaling onto neuronal survival in the ischemic retina call the putative therapeutical use of P2Y1-antagonists into question.
[Show abstract][Hide abstract] ABSTRACT: Birds which possess high visual acuity, such as eagles and falcons, are known to have retinas with a deep conically curved central foveal pit. There have been different attempts to explain the importance of this particular shape of the fovea in visual resolution. Recently, the function of Müller cells as "light fibers" was discovered, showing how the endfeet of Müller cells trap the light and then transfer it to a single cone photoreceptor. Here we describe how the endfeet of Müller cells line the walls of the foveal pit in the Pied Flycatcher, and how the Müller cell body extends its processes towards individual cones, forming machinery that could allow for light transfer from the pit wall to the photoreceptor layer alongside the pit. We describe how this construction may send an image from the fovea to the cones, and also, how the angular positioning of Müller cells, being optical extensions of the cones, has the advantage of being much denser than on a flat or slightly curved fovea. We, therefore, suggest that this type of optic fiber alignment can be used as a novel type of "amplifying array" that simply increases the amount of megapixels at the photoreceptor cell layer.