Proportion Of Retinal Ganglion Cells Research Articles

Low-dose radiation induces unstable gene expression in developing human iPSC-derived retinal ganglion organoids

The effects of low-dose radiation on undifferentiated cells carry important implications. However, the effects on developing retinal cells remain unclear. Here, we analyzed the gene expression characteristics of neuronal organoids containing immature human retinal cells under low-dose radiation and predicted their changes. Developing retinal cells generated from human induced pluripotent stem cells (iPSCs) were irradiated with either 30 or 180 mGy on days 4–5 of development for 24 h. Genome-wide gene expression was observed until day 35. A knowledge-based pathway analysis algorithm revealed fluctuations in Rho signaling and many other pathways. After a month, the levels of an essential transcription factor of eye development, the proportion of paired box 6 (PAX6)-positive cells, and the proportion of retinal ganglion cell (RGC)-specific transcription factor POU class 4 homeobox 2 (POU4F2)-positive cells increased with 30 mGy of irradiation. In contrast, they decreased after 180 mGy of irradiation. Activation of the “development of neurons” pathway after 180 mGy indicated the dedifferentiation and development of other neural cells. Fluctuating effects after low-dose radiation exposure suggest that developing retinal cells employ hormesis and dedifferentiation mechanisms in response to stress.

An In Vitro Model of Diabetic Retinal Vascular Endothelial Dysfunction and Neuroretinal Degeneration.

Background Diabetic retinopathy (DR) is a leading cause of blindness in working-age populations. Proper in vitro DR models are crucial for exploring pathophysiology and identifying novel therapeutic targets. This study establishes a rational in vitro diabetic retinal neuronal-endothelial dysfunction model and a comprehensive downstream validation system. Methods Human retinal vascular endothelial cells (HRMECs) and retinal ganglion cells (RGCs) were treated with different glucose concentrations with mannitol as matched osmotic controls. Cell proliferation and viability were evaluated by the Cell Counting Kit-8. Cell migration was measured using a transwell migration assay. Cell sprouting was assessed by a tube formation assay. The VEGF expression was assessed by ELISA. RGCs were labeled by neurons and RGC markers TUJ1 and BRN3A for quantitative and morphological analysis. Apoptosis was detected using PI/Hoechst staining and TUNEL assay and quantified by ImageJ. Results Cell proliferation and migration in HRMECs were significantly higher in the 25 mM glucose-treated group (p < 0.001) but lower in the 50 mM and 100 mM groups (p < 0.001). The permeability and the apoptotic index in HRMECs were statistically higher in the 25 mM, 50 mM, and 100 mM groups (p < 0.05). The tube formation assay found that all the parameters were significantly higher in the 25 mM and 50 mM groups (p < 0.001) concomitant with the elevated VEGFA expression in HRMECs (p = 0.016). Cell viability was significantly lower in the 50 mM, 100 mM, and 150 mM groups in RGCs (p50mM = 0.013, p100mM = 0.019, and p150mM = 0.002). Apoptosis was significantly elevated, but the proportion of RGCs with neurite extension was significantly lower in the 50 mM, 100 mM, and 150 mM groups (p50mM < 0.001, p100mM < 0.001, and p150mM < 0.001). Conclusions We have optimized glucose concentrations to model diabetic retinal endothelial (25-50 mM) or neuronal (50-100 mM) dysfunction in vitro, which have a wide range of downstream applications.

Evaluation of Macular and Retinal Ganglion Cell Count Estimates for Detecting and Staging Glaucoma.

Purpose: To investigate the clinical significance of macular estimated retinal ganglion cell (mRGC) and estimated retinal ganglion cell (eRGC) in the diagnosis and staging of glaucoma.Methods: This is a cross-section study. All enrolled subjects underwent standard automated perimetry (SAP) and optical coherence tomography (OCT) examination. Swedish Interactive Threshold Algorithm (SITA)-FAST detection strategy and 24-2, 10-2 detection programs were employed in SAP assessment. The visual-field parameters and OCT parameters were calculated according to three formulas to obtain the eRGC and mRGC1 or mRGC2. The efficiency of eRGC, mRGC1, and mRGC2 estimates for the staging of glaucoma was compared. The sensitivity and specificity of each parameter for diagnosis of glaucoma were analyzed using the receiver operating characteristic (ROC) curve.Results: A total of 119 eyes were included in the analysis. Compared with the healthy controls, eRGC, mRGC1, and mRGC2 estimates were significantly decreased in patients with glaucoma. As glaucoma progressed, eRGC, mRGC1, and mRGC2 estimates were gradually reduced. In preperimetric glaucoma, mRGC1, mRGC2, and eRGC were reduced by 13.2, 14.5, and 18%, respectively. In the mild stage of glaucoma, mRGC1, mRGC2, and eRGC were reduced by 28, 34, and 38%, respectively. In the advanced stage of glaucoma, mRGC1, mRGC2, and eRGC were reduced by 81, 85, and 92% respectively. The proportion of retinal ganglion cell (RGC) loss in the macula was close to that outside the macula. The specificity at 95% gave a sensitivity of 95.51, 86.52, and 87.64% for eRGC, mRGC1, and mRGC2, respectively. The sensitivity of structural parameters macular ganglion cell complex thickness and retinal nerve fiber layer (RNFL) were 98.88 and 95.51%, respectively. The sensitivity of functional parameters mean deviation (24-2) and visual field index (VFI) were 80.90 and 73.03%, respectively. The area under ROC curve of mRGC1, mRGC2, and eRGC were 0.982, 0.972, and 0.995 (P < 0.0001), respectively.Conclusion: Estimated retinal ganglion cell, mRGC1, and mRGC2 provide value to the staging of glaucoma and better diagnostic performance. Macular RGC estimatesthat integration of both structural and functional damages in macular may serve as a sensitive indicator for assessing macular damage in glaucoma and are of importance for the diagnosis and progression management of glaucoma.

An in vitro pressure model towards studying the response of primary retinal ganglion cells to elevated hydrostatic pressures

Glaucoma is a leading cause of blindness characterized by progressive degeneration of retinal ganglion cells (RGCs). A well-established risk factor for the development and progression of glaucoma is elevation of intraocular pressure (IOP). However, how elevated IOP leads to RGC degeneration remains poorly understood. Here, we fabricate a facile, tunable hydrostatic pressure platform to study the effect of increased hydrostatic pressure on RGC axon and total neurite length, cell body area, dendritic branching, and cell survival. The hydrostatic pressure can be adjusted by varying the height of a liquid reservoir attached to a three-dimensional (3D)-printed adapter. The proposed platform enables long-term monitoring of primary RGCs in response to various pressure levels. Our results showed pressure-dependent changes in the axon length, and the total neurite length. The proportion of RGCs with neurite extensions significantly decreased by an average of 38 ± 2% (mean ± SEM) at pressures 30 mmHg and above (p < 0.05). The axon length and total neurite length decreased at a rate of 1.65 ± 0.18 μm and 4.07 ± 0.34 μm, respectively (p < 0.001), for each mmHg increase in pressure after 72 hours pressure treatment. Dendritic branching increased by 0.20 ± 0.05 intersections/day at pressures below 25 mmHg, and decreased by 0.07 ± 0.01 intersections/day at pressures above 25 mmHg (p < 0.001). There were no significant changes in cell body area under different levels of hydrostatic pressure (p ≥ 0.05). Application of this model will facilitate studies on the biophysical mechanisms that contribute to the pathophysiology of glaucoma and provide a channel for the screening of potential pharmacological agents for neuroprotection.

Vection Responses in Patients With Early Glaucoma.

Our lab has previously shown that patients with early glaucoma have longer vection latencies than controls. We attempted to explain this finding using a combined index of structure and function (CSFI), as proposed by Medeiros and colleagues. The CSFI estimates the proportion of retinal ganglion cell loss. Roll and circular vection were evoked using a back-projected screen (experiment 1) and the Oculus Rift system (experiment 2). Vection latency and duration were measured using a button response box. In experiment 1, tilt angles were measured with a tilt sensor, whereas subjective tilt was determined using a joystick attached to a protractor. In experiment 2, subjective vection strength was rated on a 1 to 10 scale. These measurements were compared with the CSFI, which utilizes visual field and optical coherence tomography data. For experiment 1 we tested 22 patients (mean age, 70.3±6 y) with glaucoma and 18 controls (mean age, 54.6±9 y); and for experiment 2 we tested 24 patients (mean age, 71.1 ±5 y) and 23 controls (mean age 61.4±10 y), but not all patients experienced vection. In both experiments, vection latency was significantly longer for patients than for controls (smallest P=0.02). The CSFI was not related to vection latency, duration, or objective and subjective measures of vection strength (smallest P=0.06) in either experiment. Two experiments have replicated the finding that vection responses are longer in patients with glaucoma than in controls; however, the CSFI is not related to vection responses.

Caspase-2 Mediates Site-Specific Retinal Ganglion Cell Death After Blunt Ocular Injury.

Ocular trauma is common in civilian and military populations. Among other injuries, closed globe blunt ocular trauma causes acute disruption of photoreceptor outer segments (commotio retinae) and retinal ganglion cell (RGC) death (traumatic optic neuropathy [TON]), both of which permanently impair vision. Caspase-2-dependent cell death is important and evidenced in models of RGC degeneration. We assessed the role of caspase-2 as a mediator of RGC and photoreceptor death in a rat blunt ocular trauma model. Bilateral ballistic closed globe blunt ocular trauma was induced in female Lister-hooded rats and caspase-2 cleavage and localization assessed by Western blotting and immunohistochemistry. Retinal caspase-2 was knocked down by intravitreal injection of caspase-2 small interfering RNA (siCASP2). In retinal sections, RGC survival was assessed by BRN3A-positive cell counts and photoreceptor survival by outer nuclear layer (ONL) thickness, respectively. Retinal function was assessed by electroretinography (ERG). Raised levels of cleaved caspase-2 were detected in the retina at 5, 24, and 48 hours after injury and localized to RGC but not photoreceptors. Small interfering RNA-mediated caspase-2 knockdown neuroprotected RGC around but not in the center of the injury site. In addition, caspase-2 knockdown increased the amplitude of the ERG photopic negative response (PhNR) at 2 weeks after injury. However, siCASP2 was not protective for photoreceptors, suggesting that photoreceptor degeneration in this model is not mediated by caspase-2. Caspase-2 mediates death in a proportion of RGC but not photoreceptors at the site of blunt ocular trauma. Thus, intravitreally delivered siCASP2 is a possible therapeutic for the effective treatment of RGC death to prevent TON.

Functional Assessment of Melanopsin-Driven Light Responses in the Mouse: Multielectrode Array Recordings.

Intrinsically photosensitive retinal ganglion cells (ipRGCs) are a special subset of retinal output neurons capable of detecting and responding to light via a unique photopigment called melanopsin. Melanopsin activation is essential to a wide array of physiological functions, especially to those related to non-image-forming vision. Since ipRGCs only constitute a very small proportion of retinal ganglion cells, targeted recording of melanopsin-driven responses used to be a big challenge to vision researchers. Multielectrode array (MEA) recording provides a noninvasive, high throughput method to monitor melanopsin-driven responses. When synaptic inputs from rod/cone photoreceptors are silenced with glutamatergic blockers, extracellular electric signals derived from melanopsin activation can be recorded from multiple ipRGCs simultaneously by tens of microelectrodes aligned in an array. In this chapter we describe how our labs have approached MEA recording of melanopsin-driven light responses in adult mouse retinas. Instruments, tools and chemical reagents routinely used for setting up a successful MEA recording are listed, and a standard experimental procedure is provided. The implementation of this technique offers a useful paradigm that can be used to conduct functional assessments of ipRGCs and NIF vision.

Mouse retinal ganglion cell signalling is dynamically modulated through parallel anterograde activation of cannabinoid and vanilloid pathways.

Retinal cells use vanilloid transient receptor potential (TRP) channels to integrate light-evoked signals with ambient mechanical, chemical and temperature information. Localization and function of the polymodal non-selective cation channel TRPV1 (transient receptor potential vanilloid isoform 1) remains elusive. TRPV1 is expressed in a subset of mouse retinal ganglion cells (RGCs) with peak expression in the mid-peripheral retina. Endocannabinoids directly activate TRPV1 and inhibit it through cannabinoid type 1 receptors (CB1Rs) and cAMP pathways. Activity-dependent endocannabinoid release may modulate signal gain in RGCs through simultaneous manipulation of calcium and cAMP signals mediated by TRPV1 and CB1R. How retinal ganglion cells (RGCs) process and integrate synaptic, mechanical, swelling stimuli with light inputs is an area of intense debate. The nociceptive cation channel TRPV1 (transient receptor potential vanilloid type 1) modulates RGC Ca2+ signals and excitability yet the proportion of RGCs that express it remains unclear. Furthermore, TRPV1's response to endocannabinoids (eCBs), the putative endogenous retinal activators, is unknown, as is the potential modulation by cannabinoid receptors (CBRs). The density of TRPV1-expressing RGCs in the Ai9:Trpv1 reporter mouse peaked in the mid-peripheral retina. TRPV1 agonists including capsaicin (CAP) and the eCBs anandamide and N-arachidonoyl-dopamine elevated [Ca2+ ]i in 30-40% of wild-type RGCs, with effects suppressed by TRPV1 antagonists capsazepine (CPZ) and BCTC ((4-(3-chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide), and lacking in Trpv1-/- cells. The cannabinoid receptor type 1 (CB1R) colocalized with TRPV1:tdTomato expression. Its agonists 2-arachidonoylglycerol (2-AG) and WIN55,122 inhibited CAP-induced [Ca2+ ]i signals in adult, but not early postnatal, RGCs. The suppressive effect of 2-AG on TRPV1 activation was emulated by positive modulators of the protein kinase A (PKA) pathway, inhibited by the CB1R antagonist rimonabant and Gi uncoupler pertussis toxin, and absent in Cnr1-/- RGCs. We conclude that TRPV1 is a modulator of Ca2+ homeostasis in a subset of RGCs that show non-uniform distribution across the mouse retina. Non-retrograde eCB-mediated modulation of RGC signalling involves a dynamic push-pull between direct TRPV1 activation and PKA-dependent regulation of channel inactivation, with potential functions in setting the bandwidth of postsynaptic responses, sensitivity to mechanical/excitotoxic stress and neuroprotection.

Delayed neurogenesis leads to altered specification of ventrotemporal retinal ganglion cells in albino mice.

BackgroundProper binocular vision depends on the routing at the optic chiasm of the correct proportion of retinal ganglion cell (RGC) axons that project to the same (ipsilateral) and opposite (contralateral) side of the brain. The ipsilateral RGC projection is reduced in mammals with albinism, a congenital disorder characterized by deficient pigmentation in the skin, hair, and eyes. Compared to the pigmented embryonic mouse retina, the albino embryonic mouse retina has fewer RGCs that express the zinc-finger transcription factor, Zic2, which is transiently expressed by RGCs fated to project ipsilaterally. Here, using Zic2 as a marker of ipsilateral RGCs, Islet2 as a marker of contralateral RGCs, and birthdating, we investigate spatiotemporal dynamics of RGC production as they relate to the phenotype of diminished ipsilateral RGC number in the albino retina.ResultsAt embryonic day (E)15.5, fewer Zic2-positive (Zic2+) RGCs are found in the albino ventrotemporal (VT) retina compared with the pigmented VT retina, as we previously reported. However, the reduction in Zic2+ RGCs in the albino is not accompanied by a compensatory increase in Zic2-negative (Zic2−) RGCs, resulting in fewer RGCs in the VT retina at this time point. At E17.5, however, the number of RGCs in the VT region is similar in pigmented and albino retinae, implicating a shift in the timing of RGC production in the albino. Short-term birthdating assays reveal a delay in RGC production in the albino VT retina between E13 and E15. Specifically, fewer Zic2+ RGCs are born at E13 and more Zic2− RGCs are born at E15. Consistent with an increase in the production of Zic2− RGCs born at later ages, more RGCs at E17.5 express the contralateral marker, Islet2, in the albino VT retina compared with the pigmented retina.ConclusionsA delay in neurogenesis in the albino retina is linked to the alteration of RGC subtype specification and consequently leads to the reduced ipsilateral projection that characterizes albinism.

Identification of parvalbumin-containing retinal ganglion cells in rabbit

A calcium-binding protein, parvalbumin (PV), is widely distributed in the central nervous system and is expressed in the retinal neurons of various vertebrate species. The present study was aimed at describing the types and density of PV-containing retinal ganglion cells (RGCs) in rabbits by using single-cell injection after immunocytochemistry. PV-containing RGCs were first identified by immunocytochemistry and were then iontophoretically injected with a lipophilic dye, DiI. Subsequently, confocal microscopy was used to characterize the morphological classification of the PV-immunoreactive (IR) ganglion cells on the basis of their dendritic field size, branching pattern, and stratification within the inner plexiform layer. The results indicated that at least 8 morphologically different types of rabbit RGCs express PV. They were heterogeneous in terms of their morphology. The present study showed that the proportion of RGCs that contained PV was between 17% and 19% of the total number of ganglion cells. The density of PV-IR RGCs in the rabbit retina was 144 cells/mm2. Also, it was found that PV was present in all cholinergic amacrine cells in the ganglion cell layer (GCL) and the inner nuclear layer (INL). This integrated approach of characterizing the cell morphology and the selective expression of a particular protein will lead to a better understanding of the properties of RGCs.

Bcl-2 overexpression per se does not promote regeneration of neonatal crushed optic fibers.

We have explored whether overexpression of the bcl-2 gene 'per se' can promote regeneration of retinal ganglion cells (RGCs) after optic nerve axotomy in developing transgenic mice. We have used newborn mice (postnatal day 5) because at this age the central nervous system environment is more permissive for regeneration than in adults, thus, maximizing the probability to detect a regeneration-promoting role of bcl-2. Thirty days postsurgery we found that in mice overexpressing bcl-2, a high proportion of retinal ganglion cells survived and also that some fibers in the proximal stump of the optic nerve were preserved. However, the optic nerve of transgenic mice does not show signs of regeneration. On the contrary, in the presence of Schwann cell transplants, there are signs of fiber regrowth. Indeed, many axonal terminals cross the crush site and reach the chiasm in both wild type and transgenic mice nerves. These results suggest that bcl-2 overexpression is not sufficient 'per se' to increase the regenerative potentiality of axotomized RGCs.

A Key Role for GAP-43 in the Retinotectal Topographic Organization

To have a proper spatial visual perception, vertebrate retinal ganglion cells connect to their brain targets in a highly ordered fashion. The molecular bases for such topographic retinotectal connection in mammals still remain largely unknown. Using the gene knock-out approach in mice, we report here a key role for the GAP-43 growth cone protein in the development of the visual system. In mice bearing a targeted disruption of GAP-43 exon 1, a high proportion of retinal ganglion cell (RGC) axons was found to grow abnormally into the ipsilateral optic tract and into the hypothalamus. After leaving the optic chiasm during development, the GAP-43-deficient RGC axons generally follow the optic tracts but are unable to form proper terminal zones in the lateral geniculate nucleus. Moreover, in the superior colliculus, RGC axons lacking GAP-43 are intermingled. These results suggest an essential role for GAP-43 in development of the topographic retinotectal connection.

Transient neovascularisation of the frog retina during optic nerve regeneration.

In conditions such as diabetic retinopathy, degenerative events in the retina are associated with neovascularisation. It is well established that a proportion of retinal ganglion cells die during optic nerve regeneration in the frog. The present study has determined whether neovascularisation takes place during this regenerative process. To do so, the pattern of blood vessels overlying the retinal ganglion cell layer was analysed in the frog Litoria (Hyla) moorei. We examined normal animals and those undergoing optic nerve regeneration following nerve crush. Blood vessels were visualised by perfusion with Indian ink and retinae were prepared as wholeamounts. In normal animals, the vascular tree was found to lie superficial to the nerve fibre layer and was more complex in regions overlying the area centralis and visual streak. After nerve crush, abnormal blood vessels transiently formed between the existing branches of the vascular tree. The new vessels were concentrated as an annulus centred on the optic nerve head and over the area centralis in midtemporal retina. The neovascularisation became most extensive between 6 and 10 weeks postcrush and disappeared by 12 weeks. The spatiotemporal sequence of neovascularisation suggests that it is triggered by accumulations of degenerating material formed as a proportion of the ganglion cells die during optic nerve regeneration.

N-methyl-D-aspartate antagonists prevent kainate neurotoxicity in rat retinal ganglion cells in vitro

Under defined culture conditions, exogenous glutamate (Glu), NMDA, or an endogenous Glu-related toxin is lethal to rat retinal ganglion cells; these detrimental effects are NMDA receptor mediated because specific NMDA antagonists can prevent cellular injury. In the presence of an endogenous Glu-like toxin, 125 microM kainate (KA) increases the proportion of retinal ganglion cells that die, but the toxicity (due to both KA and the endogenous toxin) is totally prevented by 2-amino-5-phosphonovalerate (APV), a specific NMDA receptor antagonist. These findings indicate that the KA-induced portion of retinal ganglion cell death also appears to be mediated via NMDA receptors. There are at least 2 possible mechanisms for this lethal effect. In addition to KA receptors, KA could directly stimulate NMDA receptors. Alternatively, KA might activate its own specific receptor, which in turn leads to a net increase in the release of an endogenous Glu-related toxin; this endogenous substance would then activate NMDA receptors. Patch-clamp electrophysiology experiments have helped to distinguish between these possibilities. Concentrations of APV that completely block the current elicited by maximal nondesensitizing doses of NMDA exert no detectable inhibition of KA-evoked currents. Hence, at the concentrations used, it appears unlikely that KA directly activates NMDA receptors in this preparation. Furthermore, the fraction of toxicity attributed to the addition of KA can be blocked by the relatively specific non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). This finding is consistent with the hypothesis that KA adds an increment of toxicity in this system by directly interacting with KA receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of the initial retinal ganglion cell projection to the contralateral superior colliculus in albino and pigmented rats

Newborn albino and pigmented rats received localised Fast blue (FB) injections into the most caudal part of the contralateral superior colliculus (SC). A proportion of retinal ganglion cells (RGC's) from the temporal retina which in the adult projects exclusively to the rostral half of the colliculus are labelled by injections to the caudal colliculus in neonatal animals. The majority of these cells die during the period of naturally occurring cell death in the retina, which occurs during the first 10 postnatal days. The object of this experiment was to see whether albino rats, which have well documented abnormalities in axon pathfinding in their visual system, had a larger number of cells in temporal retina which initially project to caudal colliculus than pigmented animals. On postnatal day 2 (P2), the ratio of temporal to nasal RGCs projecting to the caudal SC is greater in albino than pigmented rats (6.2% vs 2.65%). After the wave of naturally occurring cell death, at P14, when many of the neonatal errors have been eliminated, the ratio of temporal to nasal RGC's is reduced to 1.71% for albinos versus 1.53% for pigmented rats.

Visual cortex controls retinal output in the rat

The first objective of the present investigation was to shed more light on corticofugal influences on the retina by providing an analysis of the type and proportion of retinal ganglion cells that are affected by cooling the visual cortex in rats. The second question was to determine if the pretectum participates in functional cortico-retinal relationships. In urethane-anesthetized and paralyzed hooded rats, axonal activity of retinal ganglion cells was recorded with glass micropipettes at optic chiasm level. Units were classified as ON, OFF, suppressed-by-light and concentric. The visual cortex was inactivated by cooling its surface with a 4 mm 2 steel probe using the Peltier effect. The pretectum was blocked with microinjections of 50 to 100 nanoliters of cobalt ions, lidocaine hydrochloride or KCl. The inactivations and recoveries at both sites were monitored by simultaneously recording evoked field potentials. Interrupting corticofugal impulses caused modifications of the evoked discharge pattern in all types of cells. The concentric type was the group least affected by cortical cooling. A common trend emerged suggesting that cooling of the visual cortex led to an enhancement of the initial evoked excitation. This was often followed by an enhanced post-excitatory inhibition. The Pearson coefficient allowed us to measure the degree of similarity between two histograms. When all data were pooled, a weak correlation between control and test histograms (r=0.29, N = 56) was found, while the control and recovery patterns averaged a correlation of more than twice that size (r=0.68). In a second series of experiments, the pretectum and visual cortex (VC) were simultaneously inactivated. It is shown that both sites summed their influence and acted synergistically upon the pattern of ganglion cell responses. The results strongly suggest that the visual cortex exerts a major control over the response pattern of thirty percent of retinal ganglion cells and that the pretectum participates in the functional relationships between visual cortex and retina in rats.

Suppression of maintained activity of retinal ganglion cells

Recordings were made of the changes in unit discharge rates of on-center and off-center retinal ganglion cells when the luminance of a spot in the receptive field was increased or decreased from a background level. A prolonged suppression of maintained activity to background illumination was observed in both transient and sustained cells of cat and monkey. On-units decreased in rate when the luminance of the spot was reduced: off-units decreased in rate when the luminance of the spot was increased. Long duration silence of maintained activity was dependent upon spot size, position and luminance. The most effective spots covered only the receptive field center. With low contrast levels a response time course was found which did not follow a recovery back to maintained rate along a single exponential function. Increasing contrast silenced a progressively greater proportion of retinal ganglion cells.

Magnification in Striate Cortex and Retinal Ganglion Cell Layer of Owl Monkey: A Quantitative Comparison

Magnification, the relative size of the neural representation of a portion of the visual field, decreases more rapidly with increasing visual field eccentricity in striate cortex than in the retinal ganglion cell layer of the owl monkey (Aotus trivirgatus); the proportion of the cells in striate cortex devoted to central vision is much larger than the comparable proportion of retinal ganglion cells. Magnification in striate cortex is a power function of magnification in the retinal ganglion cell layer. A formula for convergence (ganglion cells to cortical neurons) follows from this relationship.