Processes Of Ganglion Cells Research Articles

Cell-specific localization of β-synuclein in the mouse retina.

β-synuclein, a member of the synuclein family, is frequently co-expressed with α-synuclein in the neural system, where it serves to inhibit abnormal aggregation of α-synuclein in neurodegenerative diseases. Beyond its role in pathological conditions, β-synuclein plays various functions independently of α-synuclein. In our investigation, we discovered a broader expression of β-synuclein in the mouse retina compared to α-synuclein. This widespread pattern implies its potential significance in the retina. Through detailed examination via light- and electron-microscopic immunocytochemistry, we identified β-synuclein expression from the inner segment (IS) and outer segment (OS) of photoreceptor cells to the ganglion cell layer (GCL). Our findings unveiled unique features, including β-synuclein immunoreactive IS and OS of cones, higher expression in cone pedicles than in rod spherules, absence in horizontal cells, limited expression in cone bipolar dendrites and somas, higher expression in cone bipolar terminals, presence in most amacrine cells, and expression in almost majority of somas in GCL with an absence in intrinsically photosensitive retinal ganglion cell (ipRGCs) processes. Notably, all cholinergic amacrine cells express high β- but not α-synuclein, while dopaminergic amacrine cells express α-synuclein exclusively. These distinctive expression patterns offer valuable insights for further exploration into the functions of β-synuclein and its potential role in synuclein pathology within the retina.

Ginsenoside Rg1 promotes neurite growth of retinal ganglion cells through cAMP/PKA/CREB pathways

BackgroundMechanisms of synaptic plasticity in retinal ganglion cells (RGCs) are complex and the current knowledge cannot explain. Growth and regeneration of dendrites together with synaptic formation are the most important parameters for evaluating the cellular protective effects of various molecules. The effect of ginsenoside Rg1 (Rg1) on the growth of retinal ganglion cell processes has been poorly understood. Therefore, we investigated the effect of ginsenoside Rg1 on the neurite growth of RGCs. MethodsExpression of proteins and mRNA were detected by Western blot and qPCR. cAMP levels were determined by ELISA. In vivo effects of Rg1 on RGCs were evaluated by hematoxylin and eosin, and immunohistochemistry staining. ResultsThis study found that Rg1 promoted the growth and synaptic plasticity of RGCs neurite by activating the cAMP/PKA/CREB pathways. Meanwhile, Rg1 upregulated the expression of GAP43, Rac1 and PAX6, which are closely related to the growth of neurons. Meantime, H89, an antagonist of PKA, could block this effect of Rg1. In addition, we preliminarily explored the effect of Rg1 on enhancing the glycolysis of RGCs, which could be one of the mechanisms for its neuroprotective effects. ConclusionRg1 promoted neurite growth of RGCs through cAMP/PKA/CREB pathways. This study may lay a foundation for its clinical use of optic nerve diseases in the future.

The Retino-Hypothalamic Ultrastructural Changes in Traumatic Optic Neuropathy

Aim: To study the retino-hypothalamic ultrastructural changes in traumatic optic neuropathy’s pathogenesis and treatment. Methods: Four groups of mature rabbits were included in this experiment, 30 in each group, 120 in total. The traumatic crush to the optic nerves was reproduced by surgical clips to 90 mature rabbits. The first group (I) included intact/control animals, the second (II) included animals with traumatic optic neuropathy and two other traumatized groups (III and IV) who were given two different doses of treatment. The animals in group III were given infusions of Methylprednisolone 30mg/kg/day for three days. The group IV animals received infusion of 15mg/kg/ day of Methylprednisolone for 3 days in combination with phosphine electric stimulation (PES), starting from the third until the 13th day of the experiment. The electrical pulse which was used on the affected side of the animal was 800 mА and 300 mА on the opposite side. The morphological analysis of the retina and suprachiasmatic nucleus of the hypothalamus of all the four groups of animals included electron microscopy of the semi-thin and ultrathin sections. This analysis was performed a month following the initial injury while the animals were removed from the experiment. The levels of cortisol and adrenocorticotropic hormone (ACTH) in the blood of all experimental animals was tested up to one month following the injury to the optic nerves. Results: We found that trauma to the orbital part of the optic nerve causes collocative necrosis of ganglion cells and swelling of the nerve fiber layer of the ipsilateral retina. In addition, such traumatic damage causes structural changes in the suprachiasmatic nucleus of the hypothalamus. Combined treatment of methylprednisolone with phosphine electro stimulation in traumatized rabbits reduced the thickness of the retina, reduced the cytokaryometric indices and the regeneration processes of bipolar and ganglion cells of the retina. Histopathologically we found an increased number of neurosecretory granules in the suprachiasmatic nucleus of the hypothalamus. ACTH levels in the blood of the group III rabbits were found to be lower, while the cortisol levels higher, and these hormone levels in the IV group rabbits were quite similar to those of the group which was not treated. Conclusion: The combined treatment of traumatic optic neuropathy in rabbits with phosphine electrostimulation and methylprednisolone can be considered a useful treatment, having a beneficial neuroprotective effect.

Mammalian Retinal Cell Quantification.

Normal retina and its cell layers are essential for processing visual stimuli, and loss of its integrity has been documented in many disease processes. The numbers and the axonal processes of retinal ganglion cells are reduced substantially in glaucoma, leading to vision loss and blindness. Similarly, selective loss of photoreceptors in age-related macular degeneration and hereditary retinal dystrophies also results in the compromise of visual acuity. Development of genetically modified mice has led to increased understanding of the pathogenesis of many retinal diseases. Similarly, in this digital era, usage of modalities to quantify the retinal cell loss has grown exponentially leading to a better understanding of the suitability of animal models to study human retinal diseases. These quantification modalities provide valuable quantifiable data in studying pathogenesis and disease progression. This review will discuss the immunohistochemical markers for various retinal cells, available automated tools to quantify retinal cells, and present an example of retinal ganglion cell quantification using HALO image analysis platform. Additionally, we briefly review retinal cell types and subtypes, salient features of retina in various laboratory animal species, and a few of the main disease processes that affect retinal cell numbers in humans.

A Blind Stereoscopic Image Quality Evaluator with Segmented Stacked Autoencoders Considering The Whole Visual Perception Route.

Most of the current blind stereoscopic image quality assessment (SIQA) algorithms cannot show reliable accuracy. One reason is that they do not have the deep architectures and the other reason is that they are designed on the relatively weak biological basis, compared with findings on human visual system (HVS). In this paper, we propose a Deep Edge and COlor Signal INtegrity Evaluator (DECOSINE) based on the whole visual perception route from eyes to the frontal lobe, and especially focus on edge and color signal processing in retinal ganglion cells (RGC) and lateral geniculate nucleus (LGN). Furthermore, to model the complex and deep structure of the visual cortex, Segmented Stacked Auto-encoder (S-SAE) is used, which has not utilized for SIQA before. The utilization of the S-SAE complements weakness of deep learning-based SIQA metrics that require a very long training time. Experiments are conducted on popular SIQA databases, and the superiority of DECOSINE in terms of prediction accuracy and monotonicity is proved. The experimental results show that our model about the whole visual perception route and utilization of S-SAE are effective for SIQA.

Computational modelling of salamander retinal ganglion cells using machine learning approaches

Artificial vision using computational models that can mimic biological vision is an area of ongoing research. One of the main themes within this research is the study of the retina and in particular, retinal ganglion cells which are responsible for encoding the visual stimuli. A common approach to modelling the internal processes of retinal ganglion cells is the use of a linear – non-linear cascade model, which models the cell’s response using a linear filter followed by a static non-linearity. However, the resulting model is generally restrictive as it is often a poor estimator of the neuron’s response. In this paper we present an alternative to the linear – non-linear model by modelling retinal ganglion cells using a number of machine learning techniques which have a proven track record for learning complex non-linearities in many different domains. A comparison of the model predicted spike rate shows that the machine learning models perform better than the standard linear – non-linear approach in the case of temporal white noise stimuli.

Inferring hidden structure in multilayered neural circuits.

A central challenge in sensory neuroscience involves understanding how neural circuits shape computations across cascaded cell layers. Here we attempt to reconstruct the response properties of experimentally unobserved neurons in the interior of a multilayered neural circuit, using cascaded linear-nonlinear (LN-LN) models. We combine non-smooth regularization with proximal consensus algorithms to overcome difficulties in fitting such models that arise from the high dimensionality of their parameter space. We apply this framework to retinal ganglion cell processing, learning LN-LN models of retinal circuitry consisting of thousands of parameters, using 40 minutes of responses to white noise. Our models demonstrate a 53% improvement in predicting ganglion cell spikes over classical linear-nonlinear (LN) models. Internal nonlinear subunits of the model match properties of retinal bipolar cells in both receptive field structure and number. Subunits have consistently high thresholds, supressing all but a small fraction of inputs, leading to sparse activity patterns in which only one subunit drives ganglion cell spiking at any time. From the model’s parameters, we predict that the removal of visual redundancies through stimulus decorrelation across space, a central tenet of efficient coding theory, originates primarily from bipolar cell synapses. Furthermore, the composite nonlinear computation performed by retinal circuitry corresponds to a boolean OR function applied to bipolar cell feature detectors. Our methods are statistically and computationally efficient, enabling us to rapidly learn hierarchical non-linear models as well as efficiently compute widely used descriptive statistics such as the spike triggered average (STA) and covariance (STC) for high dimensional stimuli. This general computational framework may aid in extracting principles of nonlinear hierarchical sensory processing across diverse modalities from limited data.

The morphological characterization of orientation-biased displaced large-field ganglion cells in the central part of goldfish retina.

The vertebrate retina has about 30 subtypes of ganglion cells. Each ganglion cell receives synaptic inputs from specific types of bipolar and amacrine cells ramifying at the same depth of the inner plexiform layer (IPL), each of which is thought to process a specific aspect of visual information. Here, we identified one type of displaced ganglion cell in the goldfish retina which had a large and elongated dendritic field. As a population, all of these ganglion cells were oriented in the horizontal axis and perpendicular to the dorsal-ventral axis of the goldfish eye in the central part of retina. This ganglion cell has previously been classified as Type 1.2. However, the circuit elements which synapse with this ganglion cell are not yet characterized. We found that this displaced ganglion cell was directly tracer-coupled only with homologous ganglion cells at sites containing Cx35/36 puncta. We further illustrated that the processes of dopaminergic neurons often terminated next to intersections between processes of ganglion cells, close to where dopamine D1 receptors were localized. Finally, we showed that Mb1 ON bipolar cells had ribbon synapses in the axonal processes passing through the IPL and made ectopic synapses with this displaced ganglion cell that stratified into stratum 1 of the IPL. These results suggest that the displaced ganglion cell may synapse with both Mb1 cells using ectopic ribbon synapses and OFF cone bipolar cells with regular ribbon synapses in the IPL to function in both scotopic and photopic light conditions.

Synaptic Rectification Controls Nonlinear Spatial Integration of Natural Visual Inputs

A central goal in the study of any sensory system is topredict neural responses to complex inputs, especially those encountered during natural stimulation. Nowhere is the transformation from stimulus to response better understood than the vertebrate retina. Nevertheless, descriptions of retinal computation are largely based on stimulation using artificial visual stimuli, and it is unclear how these descriptions map onto the encoding of natural stimuli. We demonstrate that nonlinear spatial integration, a common feature of retinal ganglion cell (RGC) processing, shapes neural responses to natural visual stimuli in primate Off parasol RGCs, whereas On parasol RGCs exhibit surprisingly linear spatial integration. Despite this asymmetry, both cell types show strong nonlinear integration when presented with artificial stimuli. We show that nonlinear integration of natural stimuli is a consequence of rectified excitatory synaptic input and that accounting for nonlinear spatial integration substantially improves models that predict RGC responses to natural images.

NMDA and AMPA receptors contribute similarly to temporal processing in mammalian retinal ganglion cells.

Postsynaptic AMPA- and NMDA-type glutamate receptors (AMPARs, NMDARs) are commonly expressed at the same synapses. AMPARs are thought to mediate the majority of fast excitatory neurotransmission whereas NMDARs, with their relatively slower kinetics and higher Ca(2+) permeability, are thought to mediate synaptic plasticity, especially in neural circuits devoted to learning and memory. In sensory neurons, however, the roles of AMPARs and NMDARs are less well understood. Here, we tested in the in vitro guinea pig retina whether AMPARs and NMDARs differentially support temporal contrast encoding by two ganglion cell types. In both OFF Alpha and Delta ganglion cells, contrast stimulation evoked an NMDAR-mediated response with a characteristic J-shaped I-V relationship. In OFF Delta cells, AMPAR- and NMDAR-mediated responses could be modulated at low frequencies but were suppressed during 10 Hz stimulation, when responses were instead shaped by synaptic inhibition. With inhibition blocked, both AMPAR- and NMDAR-mediated responses could be modulated at 10 Hz, indicating that NMDAR kinetics do not limit temporal encoding. In OFF Alpha cells, NMDAR-mediated responses followed stimuli at frequencies up to ∼18 Hz. In both cell types, NMDAR-mediated responses to contrast modulation at 9-18 Hz showed delays of <10 ms relative to AMPAR-mediated responses. Thus, NMDARs combine with AMPARs to encode rapidly modulated glutamate release, and NMDAR kinetics do not limit temporal coding by OFF Alpha and Delta ganglion cells substantially. Furthermore, glutamatergic transmission is differentially regulated across bipolar cell pathways: in some, release is suppressed at high temporal frequencies by presynaptic inhibition.

Microglial cell reaction after optic nerve lesions

AbstractMicroglial cells may be involved in the degeneration and regeneration processes of Retinal Ganglion Cells (RGCs). Optic nerve (ON) lesions induce microglial cell activation both in goldfish (an animal with important regeneration capabilities; Salvador‐Silva et al., 2000) and rodents (animals with limited regenerating capabilities; Sobrado‐Calvo et al., 2007; Galindo‐Romero et al., 2013). The microglial cell reaction after an ON lesion is common to all the animal models studied and typically includes: increased enzyme activities, morphologic changes and cell hyperplasia. Because these reactions are found in regenerating and non‐regenerating animal models, they may represent a general response of the microglia that is directed towards helping the regeneration process. However, the location, severity and timing of the reaction varies depending on the animal model, amount of RGC death and type of lesion used and on other factors such as whether other eye lesions, trophic or other factors are administered concomitantly. Therefore the microglial cell reaction after an ON lesion can be modified externally and may subsequently influence the degeneration and regeneration processes.

Spatiotemporal flow of information in the early visual pathway

The spatial components of a visual scene are processed neurally in a sequence of coarse features followed by fine features. This coarse-to-fine temporal stream was initially considered to be a cortical function, but has recently been demonstrated in the dorsal lateral geniculate nucleus. The goal of this study was to test the hypothesis that coarse-to-fine processing is present at earlier stages of visual processing in the retinal ganglion cells that supply lateral geniculate nucleus (LGN) neurons. To compare coarse-to-fine processing in the cat's visual system, we measured the visual responses of connected neuronal pairs from the retina and LGN, and separate populations of cells from each region. We found that coarse-to-fine processing was clearly present at the ganglion cell layer of the retina. Interestingly, peak and high-spatial-frequency cutoff responses were higher in the LGN than in the retina, indicating that there was a progressive cascade of coarse-to-fine information from the retina to the LGN to the visual cortex. The analysis of early visual pathway receptive field characteristics showed that the physiological response interplay between the center and surround regions was consistent with coarse-to-fine features and may provide a primary role in the underlying mechanism. Taken together, the results from this study provided a framework for understanding the emergence and refinement of coarse-to-fine processing in the visual system.

Processing of S-cone signals in the inner plexiform layer of the mammalian retina

Color information is encoded by two parallel pathways in the mammalian retina. One pathway compares signals from long- and middle-wavelength sensitive cones and generates red-green opponency. The other compares signals from short- and middle-/long-wavelength sensitive cones and generates blue-green (yellow) opponency. Whereas both pathways operate in trichromatic primates (including humans), the fundamental, phylogenetically ancient color mechanism shared among most mammals is blue-green opponency. In this review, we summarize the current understanding of how signals from short-wavelength sensitive cones are processed in the primate and nonprimate mammalian retina, with a focus on the inner plexiform layer where bipolar, amacrine, and ganglion cell processes interact to facilitate the generation of blue-green opponency.

The effects of nicotine on cone and rod b-wave responses in larval zebrafish

Acetylcholine is present in and released from starburst amacrine cells in the inner plexiform layer (IPL), but its role in retinal function except, perhaps, in early development, is unclear. Nicotinic acetylcholine receptors are thought to be present on ganglion, amacrine, and bipolar cell processes in the IPL, and it is known that acetylcholine increases the spontaneous and light-evoked responses of retinal ganglion cells. The effects of acetylcholine on bipolar cells are not known, and here we report the effects of nicotine on the b-wave of the electroretinogram in larval zebrafish. The b-wave originates mainly from ON-bipolar cells, and the larval zebrafish retina is cone-dominated. Only small rod responses can be elicited with dim lights in wild-type larval zebrafish retinas, but rod responses can be recorded over a range of intensities in a mutant ( n o optokinetic response f ) fi sh that has no cone function. We fi nd that nicotine strongly enhances cone-driven b-wave response amplitudes but depresses rod driven b-wave response amplitudes without, however, affecting rod- or cone-driven b-wave light sensitivity.

The Peripheral Processes of Spiral Ganglion Cells After Intracochlear Application of Brain-Derived Neurotrophic Factor in Deafened Guinea Pigs

To characterize the effects of deafening and subsequent treatment with brain-derived neurotrophic factor (BDNF) on the peripheral processes (PPs) of spiral ganglion cells (SGCs) in guinea pigs. BDNF may prevent degeneration of neural structures after loss of hair cells with possible relevance for cochlear implant candidates. Guinea pigs were deafened with a combination of kanamycin and furosemide. Two weeks after deafening, intracochlear BDNF treatment was started with osmotic pumps for 4 weeks. Two weeks after cessation of BDNF treatment, the cochleae were analyzed. PPs were counted and morphologically characterized with respect to myelination, size, and shape. Deafening reduced the number of PPs. We found that BDNF treatment, started 2 weeks after deafening, significantly reduced this degenerative effect. The remaining processes showed an altered morphology; compared with normal, the size was reduced in deafened untreated animals and increased in BDNF-treated animals. The myelin sheath seemed thinner in BDNF-treated animals. We conclude that BDNF has potential as an agent that can improve the interface between cochlear implants and the auditory periphery.

KCC2-dependent subcellular ECl difference of ON-OFF retinal ganglion cells in larval zebrafish

Subcellular difference in the reversal potential of Cl− (ECl) has been found in many types of neurons. As local ECl largely determines the action of nearby GABAergic/glycinergic synapses, subcellular ECl difference can effectively regulate neuronal computation. The ON-OFF retinal ganglion cell (RGC) processes both ON and OFF visual signals via its ON and OFF dendrites, respectively. It is thus interesting to investigate whether the ON and OFF dendrites of single RGCs exhibit different local ECl. Here, using in vivo gramicidin-perforated patch recording in larval zebrafish ON-OFF RGCs, we examine local ECl at the ON and OFF dendrites, and soma through measuring light-evoked ON and OFF inhibitory responses, and GABA-induced response at the soma, respectively. We find there are subcellular ECl differences between the soma and dendrite, as well as between the ON and OFF dendrites of single RGCs. These somato-dendritic and inter-dendritic ECl differences are dependent on the Cl− extruder, K+/Cl− co-transporter (KCC2), because they are largely diminished by down-regulating kcc2 expression with morpholino oligonucleotides (MOs) or by blocking KCC2 function with furosemide. Thus, our findings indicate that there exists KCC2-dependent ECl difference between the ON and OFF dendrites of individual ON-OFF RGCs that may differentially affect visual processing in the ON and OFF pathways.

Mitochondria toxin-induced acute cochlear cell death indicates cellular activity-correlated energy consumption

The different cell types within the cochlea may have a specific contribution to the pathological changes during metabolism failure, which may provide clues for developing novel strategies for inner ear therapy. In order to evaluate activity-correlated cell death during metabolism failure in the cochlea, 3-nitropropionic acid was used to irreversibly inhibit the respiratory chain. Dose-response of the cochlear cells to 3-nitropropionic acid was analyzed in vitro. 3-Nitropropionic acid was administered onto the round window of guinea pigs. Cell death was identified by terminal transferase labeling the free 3'OH breaks in the DNA strands in vivo and propidium iodide nuclear permeation in vitro. As a result, 23.6 and 96.3 % cell death were induced by 10 and 100 mM 3-nitropropionic acid, respectively, in vitro. In the guinea pigs, 500 mM 3-nitropropionic acid induced vestibular dysfunction and severe to profound hearing losses. The cells that are the most sensitive to 3-nitropropionic acid treatment include the stria marginal and intermediate cells, epithelial cells of the Reissner's membrane, and spiral ligament fibrocytes (types II and V). Moderate sensitive cells were satellite fibrocytes of the spiral limbic central zone, osteocytes of the cochlear shell, hair cells, and spiral ganglion cells. Reduction of neurofilament in the soma and periphery processes of spiral ganglion cells occurred after the exposure. These results may be relevant to the mechanisms of injury in sudden onset sensorineural hearing loss and hazardous substance exposure-induced hearing loss.

Embryonic assembly of auditory circuits: spiral ganglion and brainstem

During early development, peripheral sensory systems generate physiological activity prior to exposure to normal environmental stimuli. This activity is thought to facilitate maturation of these neurons and their connections, perhaps even promoting efficacy or modifying downstream circuitry. In the mammalian auditory system, initial connections form at embryonic ages, but the functional characteristics of these early neural connections have not been assayed. We investigated processes of embryonic auditory development using a whole-head slice preparation that preserved connectivity between peripheral and brainstem stations of the auditory pathway. Transgenic mice expressing fluorescent protein provided observation of spiral ganglion and cochlear nucleus neurons to facilitate targeted electrophysiological recording. Here we demonstrate an apparent peripheral-to-central order for circuit maturation. Spiral ganglion cells acquire action potential-generating capacity at embryonic day 14 (E14), the earliest age tested, and action potential waveforms begin to mature in advance of comparable states for neurons of the ventral cochlear nucleus (VCN) and medial nucleus of the trapezoid body (MNTB). In accordance, auditory nerve synapses in the VCN are functional at E15, prior to VCN connectivity with the MNTB, which occurs at least 1 day later. Spiral ganglion neurons exhibit spontaneous activity at least by E14 and are able to drive third-order auditory brainstem neurons by E17. This activity precedes cochlear-generated wave activity by 4 days and ear canal opening by at least 2 weeks. Together, these findings reveal a previously unknown initial developmental phase for auditory maturation, and further implicate the spiral ganglion as a potential controlling centre in this process.

A model of retinal ganglion cell processing under natural viewing conditions.

Event Abstract Back to Event A model of retinal ganglion cell processing under natural viewing conditions. Garrett Greene1, 2*, Thomas Wachtler1, 2 and Tim Gollisch1, 3 1 BCCN München, Germany 2 LMU München, Germany 3 Georg-August-Universität Göttingen, Germany The retina is an important first stage of visual processing and is intensively studied. Little is known, however, about the retinal responses under atural viewing conditions. In particular, it is interesting to consider whether standard receptive field (RF) models can capture important features of the retinal response to complex non-stationary stimuli. We present a conceptually simple model of the peripheral visual system and investigate its behaviour under simulated eye movements. Specifically, we identify possible retinal mechanisms for rapid post-saccadic signalling as observed in several experimental studies. We model the retina as a simple photoreceptor grid which feeds forward to a retinal ganglion cell (RGC) layer consisting of numerous distinct RGC populations. We model four such populations: linear midget cells, both On-type and Off-type, and non-linear parasol cells, On-type and Off-type. Spatial receptive fields are given by a difference-of-Gaussians model. Temporal integration profiles for each population are described by the difference of two bi-phasic temporal filters which are combined with the spatial receptive field to form a rank-2 spatio-temporal filter. For midget RGCs, this filter is linearly convolved with the stimulus and rectified to generate a membrane potential. Neuronal spiking is simulated by a threshold function with non-linear feedback. Parasol cells implement a non-linear spatial integration, in which the receptive field is divided into sub-fields. Contributions from each sub-field are temporally integrated and rectified, before being summed to provide an estimate of the parasol cell membrane potential. The standard centre-surround RF can be recovered by combining sub-field RFs. The model reproduces several salient features in the reported behaviour of mammalian retina, including spatial and temporal modulation transfer functions. In addition, numerous studies have reported rapid post-saccadic bursting in retinal sub-populations. This behaviour is reproduced in our model, which displays strong transient responses to simulated saccades on a 10-ms timescale. These responses are observed primarily within our Off-type parasol population, and are less pronounced in On-type parasol cells. Midget RGCs do not display post-saccadic bursts. These differences in populations arise as a result of differing spatial and temporal integration profiles and the parasol integration non-linearity. Such dynamics are also implicated in the generation of latency codes for rapid post-saccadic processing. Our model thus captures prominent features relevant for understanding retinal processing during natural vision. Keywords: Eye Movements, retinal ganglion cell, sensory processing, Vision Conference: BC11 : Computational Neuroscience & Neurotechnology Bernstein Conference & Neurex Annual Meeting 2011, Freiburg, Germany, 4 Oct - 6 Oct, 2011. Presentation Type: Poster Topic: sensory processing (please use "sensory processing" as keyword) Citation: Greene G, Wachtler T and Gollisch T (2011). A model of retinal ganglion cell processing under natural viewing conditions.. Front. Comput. Neurosci. Conference Abstract: BC11 : Computational Neuroscience & Neurotechnology Bernstein Conference & Neurex Annual Meeting 2011. doi: 10.3389/conf.fncom.2011.53.00224 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 11 Aug 2011; Published Online: 04 Oct 2011. * Correspondence: Dr. Garrett Greene, BCCN München, München, Germany, greene@bio.lmu.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Garrett Greene Thomas Wachtler Tim Gollisch Google Garrett Greene Thomas Wachtler Tim Gollisch Google Scholar Garrett Greene Thomas Wachtler Tim Gollisch PubMed Garrett Greene Thomas Wachtler Tim Gollisch Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

DSCAM and DSCAML1 Function in Self-Avoidance in Multiple Cell Types in the Developing Mouse Retina

DSCAM and DSCAM-LIKE1 (DSCAML1) serve diverse neurodevelopmental functions, including axon guidance, synaptic adhesion, and self-avoidance, depending on the species, cell type, and gene family member studied. We examined the function of DSCAM and DSCAML1 in the developing mouse retina. In addition to a subset of amacrine cells, Dscam was expressed in most retinal ganglion cells (RGCs). RGCs had fasciculated dendrites and clumped cell bodies in Dscam(-/-) mice, suggesting a role in self-avoidance. Dscaml1 was expressed in the rod circuit, and mice lacking Dscaml1 had fasciculated rod bipolar cell dendrites and clumped AII amacrine cell bodies, also indicating a role in self-avoidance. Neurons in Dscam or Dscaml1 mutant retinas stratified their processes appropriately in synaptic laminae in the inner plexiform layer, and functional synapses formed in the rod circuit in mice lacking Dscaml1. Therefore, DSCAM and DSCAML1 function similarly in self-avoidance, and are not essential for synaptic specificity in the mouse retina.