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 Properties of multi-vesicular release from rod photoreceptors support transmission of single photon responses

2021 ◽  
Author(s):  
CL Hays ◽  
AL Sladek ◽  
GD Field ◽  
WB Thoreson
Keyword(s):  
Poisson Process ◽  
Single Photon ◽  
Glutamate Release ◽  
Bipolar Cells ◽  
Resting Membrane Potential ◽  
Rod Photoreceptors ◽  
Voltage Change ◽  
Single Photon Response ◽  
Rebound Increase ◽  
Stimulus Offset

AbstractVision under starlight requires rod photoreceptors to transduce and transmit single photon responses to the visual system. This remarkable sensitivity depends on a small voltage change reliably reducing glutamate release such that post-synaptic rod bipolar cells can robustly detect the signal. To transmit this small signal, we have found that rod vesicle release deviates strongly from a Poisson process under conditions that mimic darkness. Specifically, at their resting membrane potential in darkness, rods exhibit coordinated and regularly timed multivesicular release events. Each release event consisted of ∼17 vesicles and occurred 2-3 times more regularly than expected from a Poisson process. Hyperpolarizing rods to mimic the voltage change produced by a single photon response abruptly reduced the probability of multivesicular release nearly to zero with a rebound increase in release probability at stimulus offset. Simulations of these release dynamics indicate that this regularly timed, multivesicular release promotes transmission of single photon responses to post-synaptic neurons. Furthermore, the mechanism is efficient, requiring fewer vesicles to be released per second than uniquantal release governed by Poisson statistics.

scholarly journals Properties of multi-vesicular release from mouse rod photoreceptors support transmission of single photon responses

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Cassandra L Hays ◽  
Asia L Sladek ◽  
Greg D Field ◽  
Wallace B Thoreson
Keyword(s):  
Single Photon ◽  
Glutamate Release ◽  
Bipolar Cells ◽  
Resting Membrane Potential ◽  
Rod Photoreceptors ◽  
Poisson Statistics ◽  
Voltage Change ◽  
Vesicular Release ◽  
Rebound Increase ◽  
Stimulus Offset

Vision under starlight requires rod photoreceptors transduce and transmit single photon responses to the visual system. Small single photon voltage changes must therefore cause detectable reductions in glutamate release. We found that rods achieve this by employing mechanisms that enhance release regularity and its sensitivity to small voltage changes. At the resting membrane potential in darkness, mouse rods exhibit coordinated and regularly timed multivesicular release events, each consisting of ~17 vesicles and occurring 2-3 times more regularly than predicted by Poisson statistics. Hyperpolarizing rods to mimic the voltage change produced by a single photon abruptly reduced the probability of multivesicular release nearly to zero with a rebound increase at stimulus offset. Simulations of these release dynamics indicate that this regularly timed, multivesicular release promotes transmission of single photon responses to post-synaptic rod bipolar cells. Furthermore, the mechanism is efficient, requiring lower overall release rates than uniquantal release governed by Poisson statistics.

scholarly journals The Optimal Synapse for Sparse, Binary Signals in the Rod Pathway

2006 ◽  
Vol 18 (1) ◽  
pp. 26-44 ◽  
Author(s):  
Paul T. Clark ◽  
Mark C. W. van Rossum
Keyword(s):  
Transfer Function ◽  
Signal To Noise Ratio ◽  
Bipolar Cells ◽  
Signal To Noise ◽  
Low Light ◽  
Rod Photoreceptors ◽  
Light Levels ◽  
Noise Ratio ◽  
Simulated Images ◽  
Rod Bipolar Cells

The sparsity of photons at very low light levels necessitates a nonlinear synaptic transfer function between the rod photoreceptors and the rod-bipolar cells. We examine different ways to characterize the performance of the pathway: the error rate, two variants of the mutual information, and the signal-to-noise ratio. Simulation of the pathway shows that these approaches yield substantially different performance at very low light levels and that maximizing the signal-to-noise ratio yields the best performance when judged from simulated images. The results are compared to recent data.

Presynaptic LRIT3 Expression Trans-Synaptically Organizes Postsynaptic Trafficking of TRPM1 in Rod Bipolar Cells and Restores Vision in Dim Light

2018 ◽  
Author(s):  
Nazarul Hasan ◽  
Gobinda Pangeni ◽  
Catherine Cobb ◽  
Thomas Ray ◽  
Emily R. Nettesheim ◽  
...  
Keyword(s):  
Bipolar Cells ◽  
Dim Light ◽  
Rod Bipolar Cells

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 Activation of rod input in a model of retinal degeneration reverses retinal remodeling and induces formation of normal synapses, circuitry and visual signaling in the adult retina

2018 ◽  
Author(s):  
Tian Wang ◽  
Johan Pahlberg ◽  
Jon Cafaro ◽  
Alapakkam P. Sampath ◽  
Greg D. Field ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Retinal Ganglion Cells ◽  
Bipolar Cell ◽  
Ganglion Cells ◽  
Bipolar Cells ◽  
Mouse Retina ◽  
Retinal Ganglion ◽  
Rod Photoreceptors ◽  
Retinal Remodeling ◽  
Rod Bipolar Cells

AbstractA major cause of human blindness is the death of rod photoreceptors. As rods degenerate, synaptic structures between rod and rod bipolar cells dissolve and the rod bipolar cells extend their dendrites and occasionally make aberrant contacts. Such changes are broadly observed in blinding disorders caused by photoreceptor cell death and is thought to occur in response to deafferentation. How the remodeled retinal circuit affect visual processing following rod rescue is not known. To address this question, we generated transgenic mice wherein a disrupted cGMP-gated channel (CNG) gene can be repaired at the endogenous locus and at different stages of degeneration by tamoxifen-inducible cre-mediated recombination. In normal rods, light-induced closure of CNG channels leads to hyperpolarization of the cell, reducing neurotransmitter release at the synapse. Similarly, rods lacking CNG channel exhibit a resting membrane potential that was ~10mV hyperpolarized compared to WT rods, indicating diminished glutamate release. Retinas from these mice undergo stereotypic retinal remodeling as a consequence of rod malfunction and degeneration. Upon tamoxifen-induced expression of CNG channels, rods recovered their structure and exhibited normal light responses. Moreover, we show that the adult mouse retina displays a surprising degree of plasticity upon activation of rod input. Wayward bipolar cell dendrites establish contact with rods to support normal synaptic transmission, which is propagated to the retinal ganglion cells. These findings demonstrate remarkable plasticity extending beyond the developmental period and support efforts to repair or replace defective rods in patients blinded by rod degeneration.Significance StatementCurrent strategies for treatment of neurodegenerative disorders are focused on the repair of the primary affected cell type. However, the defective neuron functions within a complex neural circuitry, which also becomes degraded during disease. It is not known whether a rescued neuron and the remodeled circuit will establish communication to regain normal function. We show that the adult mammalian neural retina exhibits a surprising degree of plasticity following rescue of rod photoreceptors. The wayward rod bipolar cell dendrites re-establish contact with rods to support normal synaptic transmission, which is propagated to the retinal ganglion cells. These findings support efforts to repair or replace defective rods in patients blinded by rod cell loss.

scholarly journals Position of rhodopsin photoisomerization on the disk surface confers variability to the rising phase of the single photon response in vertebrate rod photoreceptors

PLoS ONE ◽  
2020 ◽  
Vol 15 (10) ◽  
pp. e0240527
Author(s):  
Giovanni Caruso ◽  
Colin J. Klaus ◽  
Heidi E. Hamm ◽  
Vsevolod V. Gurevich ◽  
Clint L. Makino ◽  
...  
Keyword(s):  
Single Photon ◽  
Disk Surface ◽  
Rod Photoreceptors ◽  
Single Photon Response
Sign in / Sign up

Export Citation Format

Share Document