scholarly journals The single-photon signal in rod bipolar cells of the dogfish retina.

1980 ◽  
Vol 300 (1) ◽  
pp. 151-166 ◽  
Author(s):  
J F Ashmore ◽  
G Falk
Keyword(s):  
Single Photon ◽  
Bipolar Cells ◽  
Photon Signal ◽  
Rod Bipolar Cells

Optimization of Single-Photon Response Transmission at the Rod-to-Rod Bipolar Synapse

Physiology ◽  
2007 ◽  
Vol 22 (4) ◽  
pp. 279-286 ◽  
Author(s):  
Haruhisa Okawa ◽  
Alapakkam P. Sampath
Keyword(s):  
Light Absorption ◽  
Single Photon ◽  
Absolute Threshold ◽  
Bipolar Cells ◽  
Physiological Mechanisms ◽  
Rod Photoreceptors ◽  
Dim Light ◽  
Single Photon Response ◽  
Rod Bipolar Cells

Our ability to see in dim light is limited by the statistics of light absorption in rod photoreceptors and the faithful transmission of the light-evoked signals through the retina. This article reviews the physiological mechanisms at the synapse between rods and rod bipolar cells, the first relay in a pathway that mediates vision near absolute threshold.

Transmission of single photon signals through a binary synapse in the mammalian retina

2004 ◽  
Vol 21 (5) ◽  
pp. 693-702 ◽  
Author(s):  
AMY BERNTSON ◽  
ROBERT G. SMITH ◽  
W. ROWLAND TAYLOR
Keyword(s):  
Ganglion Cells ◽  
Single Photon ◽  
Bipolar Cells ◽  
Single Photons ◽  
Rod Photoreceptors ◽  
Neural Noise ◽  
Light Levels ◽  
Retinal Circuitry ◽  
Binary Event ◽  
Rod Bipolar Cells

At very low light levels the sensitivity of the visual system is determined by the efficiency with which single photons are captured, and the resulting signal transmitted from the rod photoreceptors through the retinal circuitry to the ganglion cells and on to the brain. Although the tiny electrical signals due to single photons have been observed in rod photoreceptors, little is known about how these signals are preserved during subsequent transmission to the optic nerve. We find that the synaptic currents elicited by single photons in mouse rod bipolar cells have a peak amplitude of 5–6 pA, and that about 20 rod photoreceptors converge upon each rod bipolar cell. The data indicates that the first synapse, between rod photoreceptors and rod bipolar cells, signals a binary event: the detection, or not, of a photon or photons in the connected rod photoreceptors. We present a simple model that demonstrates how a threshold nonlinearity during synaptic transfer allows transmission of the single photon signal, while rejecting the convergent neural noise from the 20 other rod photoreceptors feeding into this first synapse.

scholarly journals Coordinated control of sensitivity by two splice variants of Gαo in retinal ON bipolar cells

2010 ◽  
Vol 136 (4) ◽  
pp. 443-454 ◽  
Author(s):  
Haruhisa Okawa ◽  
Johan Pahlberg ◽  
Fred Rieke ◽  
Lutz Birnbaumer ◽  
Alapakkam P. Sampath
Keyword(s):  
G Protein ◽  
Single Photon ◽  
Splice Variants ◽  
Light Response ◽  
Light Sensitivity ◽  
Bipolar Cells ◽  
Protein Activity ◽  
Α Subunit ◽  
Coordinated Action ◽  
Rod Bipolar Cells

The high sensitivity of scotopic vision depends on the efficient retinal processing of single photon responses generated by individual rod photoreceptors. At the first synapse in the mammalian retina, rod outputs are pooled by a rod “ON” bipolar cell, which uses a G-protein signaling cascade to enhance the fidelity of the single photon response under conditions where few rods absorb light. Here we show in mouse rod bipolar cells that both splice variants of the Go α subunit, Gαo1 and Gαo2, mediate light responses under the control of mGluR6 receptors, and their coordinated action is critical for maximizing sensitivity. We found that the light response of rod bipolar cells was primarily mediated by Gαo1, but the loss of Gαo2 caused a reduction in the light sensitivity. This reduced sensitivity was not attributable to the reduction in the total number of Go α subunits, or the altered balance of expression levels between the two splice variants. These results indicate that Gαo1 and Gαo2 both mediate a depolarizing light response in rod bipolar cells without occluding each other’s actions, suggesting they might act independently on a common effector. Thus, Gαo2 plays a role in improving the sensitivity of rod bipolar cells through its action with Gαo1. The coordinated action of two splice variants of a single Gα may represent a novel mechanism for the fine control of G-protein activity.

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
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