scholarly journals Rod Bipolar Cells Require Horizontal Cells for Invagination Into the Terminals of Rod Photoreceptors

2019 ◽  
Vol 13 ◽  
Author(s):  
Lena Nemitz ◽  
Karin Dedek ◽  
Ulrike Janssen-Bienhold
Physiology ◽  
2007 ◽  
Vol 22 (4) ◽  
pp. 279-286 ◽  
Author(s):  
Haruhisa Okawa ◽  
Alapakkam P. Sampath

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.


2004 ◽  
Vol 21 (5) ◽  
pp. 693-702 ◽  
Author(s):  
AMY BERNTSON ◽  
ROBERT G. SMITH ◽  
W. ROWLAND TAYLOR

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.


2006 ◽  
Vol 18 (1) ◽  
pp. 26-44 ◽  
Author(s):  
Paul T. Clark ◽  
Mark C. W. van Rossum

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.


2009 ◽  
Vol 26 (4) ◽  
pp. 365-374 ◽  
Author(s):  
MARGARET A. MacNEIL ◽  
SHERYL PURRIER ◽  
R. JARRETT RUSHMORE

AbstractThe cellular composition of the inner nuclear layer (INL) is largely conserved among mammals. Studies of rabbit, monkey, and mouse retinas have shown that bipolar, amacrine, Müller, and horizontal cells make up constant fractions of the INL (42, 35, 20, and 3%, respectively); these proportions remain relatively constant at all retinal eccentricities. The purpose of our study was to test whether the organization of cat retina is similar to that of other mammalian retinas. Fixed retinas were embedded in plastic, serially sectioned at a thickness of 1 μm, stained, and imaged at high power in the light microscope. Bipolar, amacrine, Müller, and horizontal cells were classified and counted according to established morphological criteria. Additional sets of sections were processed for protein kinase C and calretinin immunoreactivity to determine the relative fraction of rod bipolar and AII amacrine cells. Our results show that the organization of INL in the cat retina contains species-specific alterations in the composition of the INL tied to the large fraction of rod photoreceptors. Compared with other mammalian retinas, cat retinas show an expansion of the rod pathway with rod bipolar cells accounting for about 70% of all bipolar cells and AII cells accounting for nearly a quarter of all amacrine cells. Our results suggest that evolutionary pressures in cats over time have refined their retinal organization to suit its ecological niche.


2018 ◽  
Author(s):  
Tian Wang ◽  
Johan Pahlberg ◽  
Jon Cafaro ◽  
Alapakkam P. Sampath ◽  
Greg D. Field ◽  
...  

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.


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

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