Differential expression and distribution of Kir5.1 and Kir4.1 inwardly rectifying K+ channels in retina

2003 ◽  
Vol 285 (2) ◽  
pp. C260-C267 ◽  
Author(s):  
Masaru Ishii ◽  
Akikazu Fujita ◽  
Kaori Iwai ◽  
Shunji Kusaka ◽  
Kayoko Higashi ◽  
...  
Keyword(s):  
Cell Body ◽  
Müller Cells ◽  
Amacrine Cells ◽  
Distal Portion ◽  
Acid Decarboxylase ◽  
Muller Cells ◽  
Retinal Neurons ◽  
Functional Roles ◽  
Inwardly Rectifying ◽  
Specific Polyclonal Antibody

Kir5.1 is an inwardly rectifying K+ channel subunit whose functional role has not been fully elucidated. Expression and distribution of Kir5.1 in retina were examined with a specific polyclonal antibody. Kir5.1 immunoreactivity was detected in glial Müller cells and in some retinal neurons. In the Kir5.1-positive neurons the expression of glutamic acid decarboxylase (GAD65) was detected, suggesting that they may be GABAergic-amacrine cells. In Müller cells, spots of Kir5.1 immunoreactivity distributed diffusely at the cell body and in the distal portions, where Kir4.1 immunoreactivity largely overlapped. In addition, Kir4.1 immunoreactivity without Kir5.1 was strongly concentrated at the endfoot of Müller cells facing the vitreous surface or in the processes surrounding vessels. The immunoprecipitant obtained from retina with anti-Kir4.1 antibody contained Kir5.1. These results suggest that heterotetrameric Kir4.1/Kir5.1 channels may exist in the cell body and distal portion of Müller cells, whereas homomeric Kir4.1 channels are clustered in the endfeet and surrounding vessels. It is possible that homomeric Kir4.1 and heteromeric Kir4.1/Kir5.1 channels play different functional roles in the K+-buffering action of Müller cells.

scholarly journals NKCC1 Does Not Accumulate Chloride in Developing Retinal Neurons

2007 ◽  
Vol 98 (1) ◽  
pp. 266-277 ◽  
Author(s):  
Ling-Li Zhang ◽  
Eric Delpire ◽  
Noga Vardi
Keyword(s):  
Ganglion Cells ◽  
Chloride Concentration ◽  
Müller Cells ◽  
Amacrine Cells ◽  
Muller Cells ◽  
Retinal Neurons ◽  
High Concentration ◽  
Intracellular Chloride ◽  
Cellular Markers ◽  
Intracellular Chloride Concentration

GABA excites immature neurons due to their relatively high intracellular chloride concentration. This initial high concentration is commonly attributed to the ubiquitous chloride cotransporter NKCC1, which uses a sodium gradient to accumulate chloride. Here we tested this hypothesis in immature retinal amacrine and ganglion cells. Western blotting detected NKCC1 at birth and its expression first increased, then decreased to the adult level. Immunocytochemistry confirmed this early expression of NKCC1 and localized it to all nuclear layers. In the ganglion cell layer, staining peaked at P4 and then decreased with age, becoming undetectable in adult. In comparison, KCC2, the chloride extruder, steadily increased with age localizing primarily to the synaptic layers. For functional tests, we used calcium imaging with fura-2 and chloride imaging with 6-methoxy- N-ethylquinolinium iodide. If NKCC1 accumulates chloride in ganglion and amacrine cells, deleting or blocking it should abolish the GABA-evoked calcium rise. However, at P0-5 GABA consistently evoked a calcium rise that was not abolished in the NKCC1-null retinas, nor by applying high concentrations of bumetanide (NKCC blocker) for long periods. Furthermore, intracellular chloride concentration in amacrine and ganglion cells of the NKCC1-null retinas was ∼30 mM, same as in wild type at this age. This concentration was not lowered by applying bumetanide or by decreasing extracellular sodium concentration. Costaining for NKCC1 and cellular markers suggested that at P3, NKCC1 is restricted to Müller cells. We conclude that NKCC1 does not serve to accumulate chloride in immature retinal neurons, but it may enable Müller cells to buffer extracellular chloride.

K+ Channels of Müller Glial Cells in Retinal Disorders

2018 ◽  
Vol 17 (4) ◽  
pp. 255-260 ◽  
Author(s):  
Feng Gao ◽  
Lin-Jie Xu ◽  
Yuan Zhao ◽  
Xing-Huai Sun ◽  
Zhongfeng Wang
Keyword(s):  
Müller Cells ◽  
Major Type ◽  
Delayed Rectifier ◽  
Muller Cells ◽  
Bkca Channels ◽  
K Channels ◽  
Functional Changes ◽  
Physiological Properties ◽  
Retinal Disorders ◽  
Inwardly Rectifying

Background & Objective: Müller cell is the major type of glial cell in the vertebrate retina. Müller cells express various types of K+ channels, such as inwardly rectifying K+ (Kir) channels, big conductance Ca2+-activated K+ (BKCa) channels, delayed rectifier K+ channels (KDR), and transient A-type K+ channels. These K+ channels play important roles in maintaining physiological functions of Müller cells. Under some retinal pathological conditions, the changed expression and functions of K+ channels may contribute to retinal pathogenesis. Conclusion: In this article, we reviewed the physiological properties of K+ channels in retinal Müller cells and the functional changes of these channels in retinal disorders.

Rabbit retinal neurons and glia express a variety of ENaC/DEG subunits

2002 ◽  
Vol 283 (1) ◽  
pp. C126-C134 ◽  
Author(s):  
L. M. Brockway ◽  
Z.-H. Zhou ◽  
J. K. Bubien ◽  
B. Jovov ◽  
D. J. Benos ◽  
...  
Keyword(s):  
Expression Patterns ◽  
Müller Cells ◽  
Immunohistochemical Localization ◽  
Mammalian Brain ◽  
Rabbit Retina ◽  
Muller Cells ◽  
Retinal Neurons ◽  
Cellular Expression ◽  
The Central Nervous System ◽  
First Time

Some members of the epithelial Na+ channel/degenerin (ENaC/DEG) family of ion channels have been detected in mammalian brain. Therefore, we examined the RNA and protein expression of these channels in another part of the central nervous system, the rabbit retina. We next sought to demonstrate physiological evidence for an amiloride-sensitive current in Müller glia, which, on the basis of a previous study, are thought to express α-ENaC (Golestaneh N, de Kozak Y, Klein C, and Mirshahi M. Glia 33: 160–168, 2001). RT-PCR of retinal RNA revealed the presence of α-, β-, γ-, and δ-ENaC as well as acid-sensing ion channel (ASIC)1, ASIC2, ASIC3, and ASIC4. Immunohistochemical localization with antibodies against α-ENaC and β-ENaC showed labeling in Müller cells and neurons, respectively. The presence of α-ENaC, β-ENaC, and ASIC1 was detected by Western blotting. Cultured Müller cells were whole cell patch clamped. These cells exhibited an inward Na+ current that was blocked by amiloride. These data demonstrate for the first time both the expression of a variety of ENaC and ASIC subunits in the rabbit retina as well as distinct cellular expression patterns of specific subunits in neurons and glia.

Functional activity of retinal neurons and Muller cells in idiopathic full-thickness macular holes

2012 ◽  
Vol 90 ◽  
pp. 0-0
Author(s):  
M ZUEVA ◽  
V NEROEV ◽  
I TSAPENKO ◽  
P BYCHKOV ◽  
O SARYGINA
Keyword(s):  
Functional Activity ◽  
Müller Cells ◽  
Muller Cells ◽  
Full Thickness ◽  
Retinal Neurons ◽  
Macular Holes

Blockade of amiloride-sensitive sodium channels alters multiple components of the mammalian electroretinogram

2005 ◽  
Vol 22 (2) ◽  
pp. 143-151 ◽  
Author(s):  
LAURA M. BROCKWAY ◽  
DALE J. BENOS ◽  
KENT T. KEYSER ◽  
TIMOTHY W. KRAFT
Keyword(s):  
Physiological Role ◽  
Müller Cells ◽  
Müller Cell ◽  
Cell Physiology ◽  
Muller Cells ◽  
Retinal Neurons ◽  
Multiple Components ◽  
Cell Components ◽  
Slow Piii ◽  
Muller Cell

Retinal neurons and Müller cells express amiloride-sensitive Na+ channels (ASSCs). Although all major subunits of these channels are expressed, their physiological role is relatively unknown in this system. In the present study, we used the electroretinogram (ERG) recorded from anesthetized rabbits and isolated rat and rabbit retina preparations to investigate the physiological significance of ASSCs in the retina. Based upon our previous study showing expression of α-ENaC and functional amiloride-sensitive currents in rabbit Müller cells, we expected changes in Müller cell components of the ERG. However, we observed changes in other components of the ERG as well. The presence of amiloride elicited changes in all major components of the ERG; the a-wave, b-wave, and d-wave (off response) were enhanced, while there was a reduction in the amplitude of the Müller cell response (slow PIII). These results suggest that ASSCs play an important role in retinal function including neuronal and Müller cell physiology.

Expression of peptide NAP in rat retinal Müller cells prevents hypoxia-induced retinal injuries and promotes retinal neurons growth

2010 ◽  
Vol 64 (6) ◽  
pp. 417-423 ◽  
Author(s):  
Yuping Zheng ◽  
Hao Zeng ◽  
Huaning She ◽  
Hui Liu ◽  
Naixue Sun
Keyword(s):  
Müller Cells ◽  
Muller Cells ◽  
Retinal Neurons

Nitric oxide production and the expression of two nitric oxide synthases in the avian retina

2013 ◽  
Vol 30 (3) ◽  
pp. 91-103 ◽  
Author(s):  
MERVE TEKMEN-CLARK ◽  
EVANNA GLEASON
Keyword(s):  
Nitric Oxide ◽  
Müller Cells ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Horizontal Cells ◽  
No Production ◽  
Muller Cells ◽  
Double Labeling ◽  
Chicken Retina ◽  
Endothelial Nitric Oxide

AbstractNitric oxide (NO) is known to exert multiple effects on the function of many retinal neurons and their synapses. Therefore, it is equally important to understand the potential sources of NO within the retina. To explore this, we employ a combination of 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate (DAF-FM) based NO detection and immunohistochemistry for the NO synthetic enzymes, neuronal and endothelial nitric oxide synthase (nNOS and eNOS). We find DAF signals in photoreceptors, horizontal cells, amacrine cells, efferent synapses, Müller cells, and cells in the ganglion cell layer (GCL). nNOS immunoreactivity was consistent with the DAF signal with the exception that horizontal cells and Müller cells were not clearly labeled. eNOS-like immunoreactivity (eNOS-LI) was more widespread with photoreceptors, horizontal cells, occasional bipolar cells, amacrine cells, Müller cells, and cells in the GCL all showing labeling. Double labeling with antibodies raised against calretinin, syntaxin, and glutamine synthetase confirmed that horizontal cells, amacrine cells, and Müller cells (respectively) were expressing eNOS-LI. Although little or no nNOS labeling is observed in horizontal cells or Müller cells, the expression of eNOS-LI is consistent with the ability of these cells to produce NO. Together these results suggest that the capability to produce NO is widespread in the chicken retina. We propose that multiple forms of regulation for nNOS and eNOS play a role in the patterning of NO production in the chicken retina.

Müller cells in the retina of the cane toad, Bufo marinus, express neuropeptide Y-like immunoreactivity

1996 ◽  
Vol 13 (3) ◽  
pp. 501-508 ◽  
Author(s):  
Bao-Song Zhu ◽  
Ian Gibbins
Keyword(s):  
Amacrine Cell ◽  
Müller Cells ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Ultrastructural Level ◽  
Microscopic Level ◽  
Inner Plexiform Layer ◽  
Muller Cells ◽  
Light Microscopic Level ◽  
Cane Toad

AbstractWe have used light- and electron-microscopic immunohistochemistry to identify the presence of immunoreactivity to neuropeptide Y (NPY) within Müller cells in the retina of the cane toad, Bufo marinus. Müller cells containing NPY-like immunoreactivity (NPY-LI) were identified at the light-microscopic level by the coexistence with immunoreactivity to glial fibrillary acidic protein (GFAP) and at the ultrastructural level by their characteristic relationship to neuron cell bodies and processes. At the light-microscopic level, those cells which contained both NPY-LI and GFAP-LI usually had small cell bodies in the inner nuclear layer, while those cells which contained only NPY-LI were identified as large and small amacrine cells. The radially oriented primary processes in the inner plexiform layer and the vitreal end feet of GFAP-LI Müller cells also expressed NPY-LI. At the ultrastructural level, thin lamellar processes of Müller cells with NPY-LI enclosed some amacrine cell bodies in the inner nuclear layer and amacrine cell dendrites in the inner plexiform layer. These observations suggest that NPY-LI is localized in Müller cells in addition to two types of amacrine cells previously identified in the Bufo retina. This study provides the first evidence that glial elements in the vertebrate retina express NPY-LI.

Neurotransmitter-specific identification and characterization of neurons in the all-cone retina of Anolis carolinensis II: Glutamate and aspartate

1992 ◽  
Vol 9 (3-4) ◽  
pp. 313-323 ◽  
Author(s):  
David M. Sherry ◽  
Robert J. Ulshafer
Keyword(s):  
Ganglion Cell ◽  
Ganglion Cells ◽  
Müller Cells ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Anolis Carolinensis ◽  
Horizontal Cells ◽  
Inner Plexiform Layer ◽  
Muller Cells

AbstractImmunocytochemical and autoradiographic methods were used to identify neurons in the pure cone retina of the lizard (Anolis carolinensis) that are likely to employ glutamate (GLU) or aspartate (ASP) as a neurotransmitter.GLU immunocytochemistry demonstrated high levels of endogenous GLU in all cone types and numerous bipolar cells. Moderate GLU levels were found in horizontal and ganglion cells. Müller cells and most amacrine cells had very low GLU levels. GLU immunoreactivity (GLU-IR) in the cones was present from the inner segment to the synaptic pedicle. A large spherical cell type with moderate GLU-IR was identified in the proximal inner plexiform layer (IPL). These cells also contain ASP and have been tentatively identified as amacrine cells. Uptake of [3H]-L-GLU labeled all retinal layers. All cone types and Müller cells sequestered [3H]-D-ASP, a substrate specific for the GLU transporter.Anti-ASP labeling was observed in cones, horizontal cells, amacrine cells, and cells in the ganglion cell layer. ASP immunoreactivity (ASP-IR) in the cones was confined to the inner segment. One ASP-containing pyriform amacrine cell subtype ramifying in IPL sublamina b was identified.Analysis of GLU-IR, ASP-IR, and GABA-IR on serial sections indicated that there were two distinct populations of horizontal cells in the Anolis retina: one containing GABA-IR, GLU-IR, and ASP-IR; and another type containing only GLU-IR and ASP-IR. Light GLU-IR was frequently found in GABA-containing amacrine cells but ASP-IR was not.The distinct distributions of GLU and ASP may indicate distinctly different roles for these amino acids. GLU, not ASP, is probably the major neurotransmitter in the cone-biploar-ganglion cell pathway of the Anolis retina. Both GLU and ASP are present in horizontal cells and specific subpopulations of amacrine cells, but it is unclear if GLU or ASP have a neurotransmitter role in these cells.

scholarly journals Effect of Adenosine and Adenosine Receptor Antagonists on Retinal Müller Cell Inwardly Rectifying Potassium Channels under Exogenous Glutamate Stimulation

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Zhongjing Lin ◽  
Ping Huang ◽  
Shouyue Huang ◽  
Lei Guo ◽  
Xing Xu ◽  
...  
Keyword(s):  
Müller Cells ◽  
Muller Cells ◽  
Digestion Method ◽  
Expression Levels ◽  
Inwardly Rectifying Potassium Channels ◽  
Dose Dependent Decrease ◽  
Inwardly Rectifying ◽  
Dose Dependent ◽  
Papain Digestion

The vitreousness of glaucoma subjects contains elevated glutamate, and excessive extracellular glutamate is toxic to retinal neurons. Therefore, glutamate clearance is potentially impaired in the retina of glaucoma subjects. Müller cells play an important role in maintaining low extracellular levels of neurotransmitters, such as glutamate. A better understanding of the cross-talk between adenosine and glutamate may provide a better characterization of the regulatory network in Müller cells. Here, Müller cells were purified from the rat retina on postnatal day 5 using the papain digestion method. Application of increasing concentrations of glutamate (0-20 mmol/L) caused a dose-dependent decrease in the expression levels of Kir4.1, Kir2.1, GLAST, and GS. Exogenous adenosine regulated Kir channels and subsequently promoted GLAST and GS expression levels in Müller cells under exogenous glutamate stimulation. These effects were partly dependent on adenosine receptors.

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