scholarly journals Cone synapses in mammalian retinal rod bipolar cells

2018 ◽  
Vol 526 (12) ◽  
pp. 1896-1909 ◽  
Author(s):  
Ji-Jie Pang ◽  
Zhuo Yang ◽  
Roy A. Jacoby ◽  
Samuel M. Wu
Keyword(s):  
Bipolar Cells ◽  
Retinal Rod ◽  
Rod Bipolar Cells

scholarly journals Glycine Receptors and Glycinergic Synaptic Input at the Axon Terminals of Mammalian Retinal Rod Bipolar Cells

2003 ◽  
Vol 553 (3) ◽  
pp. 895-909 ◽  
Author(s):  
Jinjuan Cui ◽  
Yu‐Ping Ma ◽  
Stuart A. Lipton ◽  
Zhuo‐Hua Pan
Keyword(s):  
Synaptic Input ◽  
Bipolar Cells ◽  
Glycine Receptors ◽  
Axon Terminals ◽  
Retinal Rod ◽  
Rod Bipolar Cells

scholarly journals LIM-Homeodomain Transcription Factor LHX4 Is Required for the Differentiation of Retinal Rod Bipolar Cells and OFF-Cone Bipolar Subtypes

Cell Reports ◽  
2020 ◽  
Vol 32 (11) ◽  
pp. 108144
Author(s):  
Xuhui Dong ◽  
Hua Yang ◽  
Xiangtian Zhou ◽  
Xiaoling Xie ◽  
Dongliang Yu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Bipolar Cells ◽  
Homeodomain Transcription Factor ◽  
Retinal Rod ◽  
Rod Bipolar Cells ◽  
Lim Homeodomain

scholarly journals Functional ectopic neuritogenesis by retinal rod bipolar cells is regulated by miR-125b-5p during retinal remodeling in RCS rats

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Yan Fu ◽  
Baoke Hou ◽  
Chuanhuang Weng ◽  
Weiping Liu ◽  
Jiaman Dai ◽  
...  
Keyword(s):  
Bipolar Cells ◽  
Retinal Rod ◽  
Rcs Rats ◽  
Retinal Remodeling ◽  
Rod Bipolar Cells

Response of retinal rod bipolar cells in chronically hypoglycemic mice

2010 ◽  
Vol 68 ◽  
pp. e268
Author(s):  
Fuminobu Tamalu ◽  
Yumiko Umino ◽  
Yuning Sun ◽  
Eduardo Solessio ◽  
Shu-Ichi Watanabe ◽  
...  
Keyword(s):  
Bipolar Cells ◽  
Retinal Rod ◽  
Rod Bipolar Cells

scholarly journals Identification of PKCα-dependent phosphoproteins in mouse retina

2019 ◽  
Author(s):  
Colin M. Wakeham ◽  
Phillip A. Wilmarth ◽  
Jennifer M. Cunliffe ◽  
John E. Klimek ◽  
Gaoying Ren ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Functional Groups ◽  
Phorbol Ester ◽  
Bipolar Cells ◽  
Mouse Retina ◽  
Wild Type ◽  
Light Intensities ◽  
Retinal Rod ◽  
Wide Range ◽  
Rod Bipolar Cells

AbstractAdjusting to a wide range of light intensities is an essential feature of retinal rod bipolar cell (RBC) function. While persuasive evidence suggests this modulation involves phosphorylation by protein kinase C-alpha (PKCα), the targets of PKCα phosphorylation in the retina have not been identified. PKCα activity and phosphorylation in RBCs was examined by immunofluorescence confocal microscopy using a conformation-specific PKCα antibody and antibodies to phosphorylated PKC motifs. PKCα activity was dependent on light and expression of TRPM1, and RBC dendrites were the primary sites of light-dependent phosphorylation. PKCα-dependent retinal phosphoproteins were identified using a phosphoproteomics approach to compare total protein and phosphopeptide abundance between phorbol ester-treated wild type and PKCα knockout (PKCα-KO) mouse retinas. Phosphopeptide mass spectrometry identified over 1100 phosphopeptides in mouse retina, with 12 displaying significantly greater phosphorylation in WT compared to PKCα-KO samples. The differentially phosphorylated proteins fall into the following functional groups: cytoskeleton/trafficking (4 proteins), ECM/adhesion (2 proteins), signaling (2 proteins), transcriptional regulation (3 proteins), and homeostasis/metabolism (1 protein). Two strongly differentially expressed phosphoproteins, BORG4 and TPBG, were localized to the synaptic layers of the retina, and may play a role in PKCα-dependent modulation of RBC physiology. Data are available via ProteomeXchange with identifier PXD012906.SignificanceRetinal rod bipolar cells (RBCs), the second-order neurons of the mammalian rod visual pathway, are able to modulate their sensitivity to remain functional across a wide range of light intensities, from starlight to daylight. Evidence suggests that this modulation requires the serine/threonine kinase, PKCα, though the specific mechanism by which PKCα modulates RBC physiology is unknown. This study examined PKCα phosophorylation patterns in mouse rod bipolar cells and then used a phosphoproteomics approach to identify PKCα-dependent phosphoproteins in the mouse retina. A small number of retinal proteins showed significant PKCα-dependent phosphorylation, including BORG4 and TPBG, suggesting a potential contribution to PKCα-dependent modulation of RBC physiology.HighlightsPKCα is a major source of phosphorylation in retinal RBC dendrites and its activity in RBCs is light dependent.Proteins showing differential phosphorylation between phorbol ester-treated wild type and PKCα-KO retinas belong to the following major functional groups: cytoskeleton/trafficking (4 proteins), ECM/adhesion (2 proteins), signaling (2 proteins), transcriptional regulation (3 proteins), and homeostasis/metabolism (1 protein).The PKCα-dependent phosphoproteins, BORG4 and TPBG, are present in the synaptic layers of the retina and may be involved in PKCα-dependent modulation of RBC physiology.

Protein kinase modulation of GABAA currents in rabbit retinal rod bipolar cells

1996 ◽  
Vol 76 (5) ◽  
pp. 3070-3086 ◽  
Author(s):  
M. A. Gillette ◽  
R. F. Dacheux
Keyword(s):  
Protein Kinase ◽  
Phorbol Ester ◽  
Bipolar Cell ◽  
Kinase Inhibitor ◽  
Bipolar Cells ◽  
Calphostin C ◽  
Retinal Rod ◽  
Low Concentrations ◽  
Current Reduction ◽  
Rod Bipolar Cells

1. Protein kinase modulation of gamma-aminobutyric acid-A (GABAA)- and glycine-activated Cl- currents in freshly dissociated, morphologically identified rabbit retinal rod bipolar cells was studied under voltage clamp with the use of the whole cell patch-clamp technique. Responses to pulses of GABA and glycine were monitored before, during, and after application of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) and protein kinase C (PKC) activators, inactive analogues, and inhibitors. 2. Bath perfusion with either forskolin, an adenylate cyclase activator, or its inactive analogue, 1,9 dideoxyforskolin, reduced the GABA-activated Cl- currents by 30–50%; coapplication of N-[2-(Methylamino)ethyl]-5-isoquinolinesulfonamide hydrochloride (H-8), a PKA inhibitor, did not prevent the forskolin effects. The membrane-permeable cAMP analogues, 8-bromo-cAMP and 8-(4-Chlorophenylthio)-cAMP, and intracellularly dialyzed cAMP, did not modulate either the GABA- or glycine-activated Cl- current. Perfusion of the phosphodiesterase inhibitor 3-isobutyl-1-methylxantine (IBMX) had no direct effect on the GABA-activated current and did not alter the results with cAMP or its membrane-permeable analogues. Collectively, these results make it very unlikely that PKA represents an important mechanism of either GABAA or glycine channel modulation in the rabbit rod bipolar cell. 3. Although the isoquinoline sulfonamide protein kinase inhibitor H-8 was without discernible effect, the related compounds 1-(5-Isoquinolinesulfonyl)-2-methylpiperazine dihydrochlorine (H-7) and N-(2-Aminoethyl)-5-isoquinolinesulfonamide dihydrochloride (H-9) both dramatically reduced the GABA response. H-7 also strongly reduced the response to glycine, whereas H-8 had no effect and H-9 had an intermediate effect. Because only certain members of this inhibitor class of agents proved effective, and their effectiveness appeared unrelated to the established activity profiles, these agents probably inhibit the Cl- currents in a phosphorylation-independent manner. Direct interaction of these inhibitors with binding sites in the GABAA receptor-channel complex has been previously reported in some other preparations. 4. The phorbol ester and PKC activator phorbol 12,13 dibutyrate (PDB) led to a 35-55% reduction in the GABA-activated Cl- current of the rod bipolar cell. The broad-spectrum kinase inhibitor staurosporine, and the more PKC-specific inhibitor calphostin C, had no direct effect on GABA responses, but prevented Cl- current reduction when coapplied with PDB. Phorbol 12-myristate 13-acetate (PMA) reduced the GABA-activated current in a fashion very similar to PDB. Staurosporine and calphostin C blocked the PMA effect. No reduction of Cl- current was seen with the inactive analogue, 4-alpha-PMA, used as a control for PKC-independent phorbol ester effects. 5. PDB effectively reduced the GABA-activated Cl- current of the rod bipolar cell at low concentrations, whereas PMA had a diminished effect at low concentrations. This is consistent with the reported concentration-dependent abilities of these agents to promote translocation of PKC-alpha immunoreactivity from the membrane to the cytosolic compartment in the rabbit retinal rod bipolar cell. Collectively, the data from phorbol esters, inactive analogues, and kinase inhibitors support the existence of a PKC-mediated mechanism for GABA-activated Cl- current reduction in these cells. 6. The naphthalenesulfonamide PKC activator N-(n-Heptyl)-5-chloro-1-naphthalenesulfonamide (SC-10) also potently and reversibly reduced the GABA-activated current. Staurosporine and calphostin C eliminated this effect. When the nonhydrolyzable guanosine 5'-triphosphate (GTP) analogue guanosine 5'-O-(3-thiotriphosphate) tetralithium salt (GTP-gamma-S) replaced GTP in the recording pipette, the SC-10-mediated GABA current reduction became irreversible.(ABSTRACT TRUNCATED)

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