scholarly journals The glutamate transporter EAAT5 works as a presynaptic receptor in mouse rod bipolar cells

2006 ◽  
Vol 577 (1) ◽  
pp. 221-234 ◽  
Author(s):  
Eric Wersinger ◽  
Yannick Schwab ◽  
José-Alain Sahel ◽  
Alvaro Rendon ◽  
David V. Pow ◽  
...  
Keyword(s):  
Glutamate Transporter ◽  
Bipolar Cells ◽  
Presynaptic Receptor ◽  
Rod Bipolar Cells

scholarly journals Light-evoked glutamate transporter EAAT5 activation coordinates with conventional feedback inhibition to control rod bipolar cell output

2020 ◽  
Vol 123 (5) ◽  
pp. 1828-1837
Author(s):  
Gregory W. Bligard ◽  
James DeBrecht ◽  
Robert G. Smith ◽  
Peter D. Lukasiewicz
Keyword(s):  
Amino Acid ◽  
Feedback Inhibition ◽  
Excitatory Amino Acid ◽  
Glutamate Transporter ◽  
Bipolar Cells ◽  
Major Contributor ◽  
Excitatory Amino Acid Transporter ◽  
Control Rod ◽  
Neuronal Output ◽  
Rod Bipolar Cells

Excitatory amino acid transporter 5 (EAAT5) glutamate transporters have a chloride channel that is strongly activated by glutamate, which modulates excitatory signaling. We found that EAAT5 is a major contributor to feedback inhibition on rod bipolar cells. Inhibition to rod bipolar cells is also mediated by GABA and glycine. GABA and glycine mediate the early phase of feedback inhibition, and EAAT5 mediates a more delayed inhibition. Together, inhibitory transmitters and EAAT5 coordinate to mediate feedback inhibition, controlling neuronal output.

scholarly journals Mechanisms Underlying Lateral GABAergic Feedback onto Rod Bipolar Cells in Rat Retina

2010 ◽  
Vol 30 (6) ◽  
pp. 2330-2339 ◽  
Author(s):  
A. E. Chavez ◽  
W. N. Grimes ◽  
J. S. Diamond
Keyword(s):  
Bipolar Cells ◽  
Rat Retina ◽  
Rod Bipolar Cells

The rod bipolar cell of the mammalian retina

1991 ◽  
Vol 7 (1-2) ◽  
pp. 99-112 ◽  
Author(s):  
Heinz Wässle ◽  
Masayuki Yamashita ◽  
Ursula Greferath ◽  
Ulrike Grünert ◽  
Frank Müller
Keyword(s):  
Chloride Channels ◽  
Light Stimulus ◽  
Bipolar Cells ◽  
Immunocytochemical Staining ◽  
Nonselective Cation Channel ◽  
Light Responses ◽  
Kinase C ◽  
Mammalian Retina ◽  
Approaches To Study ◽  
Rod Bipolar Cells

AbstractThree approaches to study the function of mammalian rod bipolar cells are described. Extracellular recordings from the intact cat eye under light- and dark-adapted conditions showed that in dark-adapted retina all light responses can be blocked by 2-amino-4-phosphonobutyrate (APB). Immunocytochemical staining with an antibody against protein kinase C (PKC) labeled rod bipolar cells in all mammalian retinae tested. When rat retinae were dissociated, PKC immunoreactivity was also found in isolated bipolar cells and could be used for their identification as rod bipolars. Patch-clamp recordings were performed from such dissociated rod bipolar cells and their responses to APB were measured. APB closed a nonselective cation channel in the cell membrane. The actions of GABA and glycine were also tested and both opened chloride channels in dissociated rod bipolar cells. These results suggest that rod bipolar cells are depolarized by a light stimulus and that GABA as well as glycine modulate their light responses.

scholarly journals The Effect of PKCα on the Light Response of Rod Bipolar Cells in the Mouse Retina

2015 ◽  
Vol 56 (8) ◽  
pp. 4961 ◽  
Author(s):  
Wei-Hong Xiong ◽  
Ji-Jie Pang ◽  
Mark E. Pennesi ◽  
Robert M. Duvoisin ◽  
Samuel M. Wu ◽  
...  
Keyword(s):  
Light Response ◽  
Bipolar Cells ◽  
Mouse Retina ◽  
Rod Bipolar Cells

Membrane currents evoked by ionotropic glutamate receptor agonists in rod bipolar cells in the rat retinal slice preparation

1996 ◽  
Vol 76 (1) ◽  
pp. 401-422 ◽  
Author(s):  
E. Hartveit
Keyword(s):  
Nmda Receptor ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Inner Plexiform Layer ◽  
Receptor Agonists ◽  
Long Latency ◽  
Glutamate Receptor Agonists ◽  
Conductance Increase ◽  
Rod Bipolar Cells

1. With the use of the whole cell voltage-clamp technique, I have recorded the current responses to ionotropic glutamate receptor agonists of rod bipolar cells in vertical slices of rat retina. Rod bipolar cells constitute a single population of cells and were visualized by infrared differential interference contrast video microscopy. They were targeted by the position of their cell bodies in the inner nuclear layer and, after recording, were visualized in their entirety by labeling with the fluorescent dye Lucifer yellow, which was included in the recording pipette. To study current-voltage relationships of evoked currents, voltage-gated potassium currents were blocked by including Cs+ and tetraethylammonium+ in the recording pipette. 2. Pressure application of the non-N-methyl-D-aspartate (non-NMDA) receptor agonists kainate and (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) from puffer pipettes evoked a long-latency conductance increase selective for chloride ions. When the intracellular chloride concentration was increased, the reversal potential changed, corresponding to the change in equilibrium potential for chloride. The response was evoked in the presence of 5 mM Co2+ and nominally O mM Ca2+ in the extracellular solution, presumably blocking all external Ca2(+)-dependent release of neurotransmitter. 3. The long latency of kainate-evoked currents in bipolar cells contrasted with the short-latency currents evoked by gamma-aminobutyric acid (GABA) and glycine in rod bipolar cells and by kainate in amacrine cells. 4. Application of NMDA evoked no response in rod bipolar cells. 5. Coapplication of AMPA with cyclothiazide, a blocker of agonist-evoked desensitization of AMPA receptors, enhanced the conductance increase compared with application of AMPA alone. Coapplication of the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione blocked the response to kainate and AMPA, indicating that the response was mediated by conventional ionotropic glutamate receptors. 6. The conductance increase evoked by non-NMDA receptor agonists could not be blocked by a combination of 100 microM picrotoxin and 10 microM strychnine. Application of the GABAC receptor antagonist 3-aminopropyl (methyl)phosphinic acid (3-APMPA) strongly reduced the response, and coapplication of 500 microM 3-APMPA and 100 microM picrotoxin completely blocked the response. These results suggested that the conductance increase evoked by non-NMDA receptor agonists was mediated by release of GABA and activation of GABAC receptors, and most likely also GABAA receptors, on rod bipolar cells. 7. Kainate responses like those described above could not be evoked in bipolar cells in which the axon had been cut somewhere along its passage to the inner plexiform layer during the slicing procedure. This suggests that the response was dependent on the integrity of the axon terminal in the inner plexiform layer, known to receive GABAergic synaptic input from amacrine cells. 8. The results indicate that ionotropic glutamate receptors are not involved in mediating synaptic input from photoreceptors to rod bipolar cells and that an unconventional mechanism of GABA release from amacrine cells might operate in the inner plexiform layer.

CREB-induced transcriptional activation depends on mGluR6 in rod bipolar cells

1998 ◽  
Vol 57 (2) ◽  
pp. 241-247 ◽  
Author(s):  
Kazuhiko Yoshida ◽  
Junko Imaki ◽  
Yoshichika Okamoto ◽  
Hideki Iwakabe ◽  
Hitoshi Fujisawa ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Bipolar Cells ◽  
Rod Bipolar Cells

scholarly journals Diverse Mechanisms Underlie Glycinergic Feedback Transmission onto Rod Bipolar Cells in Rat Retina

2008 ◽  
Vol 28 (31) ◽  
pp. 7919-7928 ◽  
Author(s):  
A. E. Chavez ◽  
J. S. Diamond
Keyword(s):  
Bipolar Cells ◽  
Rat Retina ◽  
Rod Bipolar Cells

scholarly journals Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells

2018 ◽  
Vol 120 (2) ◽  
pp. 867-879 ◽  
Author(s):  
Michael D. Flood ◽  
Johnnie M. Moore-Dotson ◽  
Erika D. Eggers
Keyword(s):  
Light Adaptation ◽  
Amacrine Cell ◽  
Amacrine Cells ◽  
Receptor Activation ◽  
Bipolar Cells ◽  
D1 Receptor ◽  
D1 Receptors ◽  
Light Responses ◽  
Dopamine Modulation ◽  
Rod Bipolar Cells

Dopamine modulation of retinal signaling has been shown to be an important part of retinal adaptation to increased background light levels, but the role of dopamine modulation of retinal inhibition is not clear. We previously showed that light adaptation causes a large reduction in inhibition to rod bipolar cells, potentially to match the decrease in excitation after rod saturation. In this study, we determined how dopamine D1 receptors in the inner retina contribute to this modulation. We found that D1 receptor activation significantly decreased the magnitude of inhibitory light responses from rod bipolar cells, whereas D1 receptor blockade during light adaptation partially prevented this decline. To determine what mechanisms were involved in the modulation of inhibitory light responses, we measured the effect of D1 receptor activation on spontaneous currents and currents evoked from electrically stimulating amacrine cell inputs to rod bipolar cells. D1 receptor activation decreased the frequency of spontaneous inhibition with no change in event amplitudes, suggesting a presynaptic change in amacrine cell activity in agreement with previous reports that rod bipolar cells lack D1 receptors. Additionally, we found that D1 receptor activation reduced the amplitude of electrically evoked responses, showing that D1 receptors can modulate amacrine cells directly. Our results suggest that D1 receptor activation can replicate a large portion but not all of the effects of light adaptation, likely by modulating release from amacrine cells onto rod bipolar cells. NEW & NOTEWORTHY We demonstrated a new aspect of dopaminergic signaling that is involved in mediating light adaptation of retinal inhibition. This D1 receptor-dependent mechanism likely acts through receptors located directly on amacrine cells, in addition to its potential role in modulating the strength of serial inhibition between amacrine cells. Our results also suggest that another D2/D4 receptor-dependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

scholarly journals Synaptic vesicle dynamics in mouse rod bipolar cells

2008 ◽  
Vol 25 (4) ◽  
pp. 523-533 ◽  
Author(s):  
QUN-FANG WAN ◽  
ALEJANDRO VILA ◽  
ZHEN-YU ZHOU ◽  
RUTH HEIDELBERGER
Keyword(s):  
Synaptic Vesicle ◽  
Time Constant ◽  
Active Zone ◽  
Bipolar Cell ◽  
Visual Information ◽  
Membrane Surface ◽  
Bipolar Cells ◽  
Calcium Dependent ◽  
Vesicle Dynamics ◽  
Rod Bipolar Cells

AbstractTo better understand synaptic signaling at the mammalian rod bipolar cell terminal and pave the way for applying genetic approaches to the study of visual information processing in the mammalian retina, synaptic vesicle dynamics and intraterminal calcium were monitored in terminals of acutely isolated mouse rod bipolar cells and the number of ribbon-style active zones quantified. We identified a releasable pool, corresponding to a maximum of ≈35 vesicles/ribbon-style active zone. Following depletion, this pool was refilled with a time constant of ≈7 s. The presence of a smaller, rapidly releasing pool and a small, fast component of refilling was also suggested. Following calcium channel closure, membrane surface area was restored to baseline with a time constant that ranged from 2 to 21 s depending on the magnitude of the preceding Ca2+ transient. In addition, a brief, calcium-dependent delay often preceded the start of onset of membrane recovery. Thus, several aspects of synaptic vesicle dynamics appear to be conserved between rod-dominant bipolar cells of fish and mammalian rod bipolar cells. A major difference is that the number of vesicles available for release is significantly smaller in the mouse rod bipolar cell, both as a function of the total number per neuron and on a per active zone basis.

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