scholarly journals Interspike Interval Analysis of Retinal Ganglion Cell Receptive Fields

2007 ◽  
Vol 98 (2) ◽  
pp. 911-919 ◽  
Author(s):  
Daniel L. Rathbun ◽  
Henry J. Alitto ◽  
Theodore G. Weyand ◽  
W. Martin Usrey

The interspike interval (ISI) preceding a retinal spike has a strong influence on whether retinal spikes will drive postsynaptic responses in the lateral geniculate nucleus (LGN). This ISI-based filtering of retinal spikes could, in principle, be used as a mechanism for processing visual information en route from retina to cortex; however, this form of processing has not been previously explored. Using a white noise stimulus and reverse correlation analysis, we compared the receptive fields associated with retinal spikes over a range of ISIs (0–120 ms). Results showed that, although the location and sign of retinal ganglion cell receptive fields are invariant to ISI, the size and amplitude of receptive fields vary with ISI. These results support the notion that ISI-based filtering of retinal spikes can serve as a mechanism for shaping receptive fields.

Development ◽  
2021 ◽  
Author(s):  
Si Chen ◽  
Kira L. Lathrop ◽  
Takaaki Kuwajima ◽  
Jeffrey M. Gross

Visual information is transmitted from the eye to the brain along the optic nerve, a structure composed of retinal ganglion cell (RGC) axons. The optic nerve is highly vulnerable to damage in neurodegenerative diseases like glaucoma and there are currently no FDA-approved drugs or therapies to protect RGCs from death. Zebrafish possess remarkable neuroprotective and regenerative abilities and here, utilizing an optic nerve transection (ONT) injury and an RNA-seq-based approach, we identify genes and pathways active in RGCs that may modulate their survival. Through pharmacological perturbation, we demonstrate that JAK/STAT pathway activity is required for RGC survival after ONT. Furthermore, we show that immune responses directly contribute to RGC death after ONT; macrophages/microglia are recruited to the retina and blocking neuroinflammation or depleting these cells after ONT rescues survival of RGCs. Taken together, these data support a model in which crosstalk between macrophages/microglia and RGCs, mediated by Jak/Stat pathway activity, regulates RGC survival after optic nerve injury.


2018 ◽  
Author(s):  
Daniel Rathbun ◽  
Nima Ghorbani ◽  
Hamed Shabani ◽  
Eberhart Zrenner ◽  
Zohreh Hosseinzadeh

Bionic retinal implants are gaining acceptance in the treatment of blindness from degenerative diseases including retinitis pigmentosa and macular degeneration. A current obstacle to the improved performance of such implants is the difficulty of comparing the results of disparate experiments. Another obstacle is the current difficulty in selectively activating the many different retinal ganglion cell types that are used as separate pathways for visual information to the brain. To address these obstacles, we propose a modelling framework based on white noise stimulation and reverse correlation.In this perspective, we first outline early developments in visual retinal physiology leading up to the implementation of white noise stimuli and spike-triggered averaging. We then review recent efforts to adapt the white noise method for electrical stimulation of the retina and some of the nuances of this approach. Based on such white noise methods, we describe a modelling framework whereby the effect of any arbitrary electrical stimulus on a ganglion cell’s neural code can be better understood. This framework should additionally disentangle the effects of stimulation on photoreceptor, bipolar cell and retinal ganglion cell – ultimately supporting selective stimulation of specific ganglion cell types for a more nuanced bionic retinal implant. Finally, we point to upcoming considerations in this rapidly developing domain of research.


2017 ◽  
Vol 131 ◽  
pp. 96-105 ◽  
Author(s):  
Cameron S. Cowan ◽  
Jasdeep Sabharwal ◽  
Robert L. Seilheimer ◽  
Samuel M. Wu

2020 ◽  
Author(s):  
Nadia Parmhans ◽  
Anne Drury Fuller ◽  
Eileen Nguyen ◽  
Katherine Chuang ◽  
David Swygart ◽  
...  

AbstractMembers of the POU4F/Brn3 transcription factor family have an established role in the development of retinal ganglion cell types (RGCs), the projection sensory neuron conveying visual information from the mammalian eye to the brain. Our previous work using sparse random recombination of a conditional knock-in reporter allele expressing Alkaline Phosphatase (AP) and intersectional genetics had identified three types of Pou4f3/Brn3c positive (Brn3c+) RGCs. Here, we describe a novel Brn3cCre mouse allele generated by serial Dre to Cre recombination. We use this allele to explore the expression overlap of Brn3c with Brn3a and Brn3b and the dendritic arbor morphologies and visual stimulus properties of Brn3c+ RGC types. Furthermore, we explore Brn3c-expressing brain nuclei. Our analysis reveals a much larger number of Brn3c+ RGCs and more diverse set of RGC types than previously reported. The majority of RGCs having expressed Brn3c during development are still Brn3c positive in the adult, and all of them express Brn3a while only about half express Brn3b. Intersection of Brn3b and Brn3c expression highlights an area of increased RGC density, similar to an area centralis, corresponding to part of the binocular field of view of the mouse. Brn3c+ neurons and projections are present in multiple brain nuclei. Brn3c+ RGC projections can be detected in the Lateral Geniculate Nucleus (LGN), Pretectal Area (PTA) and Superior Colliculus (SC) but also in the thalamic reticular nucleus (TRN), a visual circuit station that was not previously described to receive retinal input. Most Brn3c+ neurons of the brain are confined to the pretectum and the dorsal midbrain. Amongst theses we identify a previously unknown Brn3c+ subdivision of the deep mesencephalic nucleus (DpMe). Thus, our newly generated allele provides novel biological insights into RGC type classification, brain connectivity and midbrain cytoarchitectonic, and opens the avenue for specific characterization and manipulation of these structures.


2004 ◽  
Vol 92 (1) ◽  
pp. 468-476 ◽  
Author(s):  
Dario L. Ringach

The receptive fields of simple cells in visual cortex are composed of elongated on and off subregions. This spatial arrangement is widely thought to be responsible for the generation of orientation selectivity. Neurons with similar orientation preferences cluster in “columns” that tile the cortical surface and form a map of orientation selectivity. It has been proposed that simple cell receptive fields are constructed by the selective pooling of geniculate receptive fields aligned in space. A recent analysis of monosynaptic connections between geniculate and cortical neurons appears to reveal the existence of “wiring rules” that are in accordance with the classical model. The precise origin of the orientation map is unknown, but both genetic and activity-dependent processes are thought to contribute. Here, we put forward the hypothesis that statistical sampling from the retinal ganglion cell mosaic may contribute to the generation of simple cells and provide a blueprint for orientation columns. Results from computer simulations show that the “haphazard wiring” model is consistent with data on the probability of monosynaptic connections and generates orientation columns and maps resembling those found in the cortex. The haphazard wiring hypothesis could be tested by measuring the correlation between the orientation map and the structure of the retinal ganglion cell mosaic of the contralateral eye.


2005 ◽  
Vol 94 (2) ◽  
pp. 1048-1056 ◽  
Author(s):  
Michael A. Freed

A retinal ganglion cell receives information about a white-noise stimulus as a flickering pattern of glutamate quanta. The ganglion cell reencodes this information as brief bursts of one to six spikes separated by quiescent periods. When the stimulus is repeated, the number of spikes in a burst is highly reproducible (variance < mean) and spike timing is precise to within 10 ms, leading to an estimate that each spike encodes about 2 bits. To understand how the ganglion cell reencodes information, we studied the quantal patterns by repeating a white-noise stimulus and recording excitatory currents from a voltage-clamped, brisk-sustained ganglion cell. Quanta occurred in synchronous bursts of 3 to 65; the resulting postsynaptic currents summed to form excitatory postsynaptic currents (EPSCs). The number of quanta in an EPSC was only moderately reproducible (variance = mean), quantal timing was precise to within 14 ms, and each quantum encoded 0.1–0.4 bit. In conclusion, compared to a spike, a quantum has similar temporal precision, but is less reproducible and encodes less information. Summing multiple quanta into discrete EPSCs improves the reproducibility of the overall quantal pattern and contributes to the reproducibility of the spike train.


Perception ◽  
10.1068/p5447 ◽  
2005 ◽  
Vol 34 (11) ◽  
pp. 1375-1397 ◽  
Author(s):  
Peter H Schiller ◽  
Christina E Carvey

The Hermann grid illusion consists of smudges perceived at the intersections of a white grid presented on a black background. In 1960 the effect was first explained by a theory advanced by Baumgartner suggesting the illusory effect is due to differences in the discharge characteristics of retinal ganglion cells when their receptive fields fall along the intersections versus when they fall along non-intersecting regions of the grid. Since then, others have claimed that this theory might not be adequate, suggesting that a model based on cortical mechanisms is necessary [Lingelbach et al, 1985 Perception14(1) A7; Spillmann, 1994 Perception23 691–708; Geier et al, 2004 Perception33 Supplement, 53; Westheimer, 2004 Vision Research44 2457–2465]. We present in this paper the following evidence to show that the retinal ganglion cell theory is untenable: (i) varying the makeup of the grid in a manner that does not materially affect the putative differential responses of the ganglion cells can reduce or eliminate the illusory effect; (ii) varying the grid such as to affect the putative differential responses of the ganglion cells does not eliminate the illusory effect; and (iii) the actual spatial layout of the retinal ganglion cell receptive fields is other than that assumed by the theory. To account for the Hermann grid illusion we propose an alternative theory according to which the illusory effect is brought about by the manner in which S1 type simple cells (as defined by Schiller et al, 1976 Journal of Neurophysiology39 1320–1333) in primary visual cortex respond to the grid. This theory adequately handles many of the facts delineated in this paper.


2018 ◽  
Author(s):  
Colleen E. Rhoades ◽  
Nishal P. Shah ◽  
Michael B. Manookin ◽  
Nora Brackbill ◽  
Alexandra Kling ◽  
...  

SummaryThe visual functions of the diverse retinal ganglion cell types in the primate retina, and the parallel visual pathways they initiate, remain poorly understood. Here, the unusual physiological and computational properties of the ON and OFF smooth monostratified (SM) ganglion cells are explored. Large-scale multi-electrode recordings from 48 macaque retinas revealed that these cells exhibited strikingly irregular receptive field structure composed of spatially segregated hotspots, quite different from the receptive fields of previously described retinal ganglion cell types. The ON and OFF SM cells are paired cell types, but OFF SM cells exhibited stronger hotspot structure than ON cells. Targeted visual stimulation and computational inference demonstrate strong nonlinear subunit properties of each hotspot that contributed to the signaling properties of SM cells. Analysis of shared inputs to neighboring SM cells indicated that each hotspot could not be explained by an individual presynaptic input. Surprisingly, visual stimulation of different hotspots produced subtly different spatiotemporal spike waveforms in the same SM cell, consistent with a dendritic contribution to hotspot structure. These findings point to a previously unreported nonlinear mechanism in the output of the primate retina that contributes to signaling spatial information.


Sign in / Sign up

Export Citation Format

Share Document