Retinal Ganglion Cell Soma Research Articles

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.

In Vivo Imaging of Retinal Ganglion Cell Axons within the Nerve Fiber Layer

Purpose. Optic nerve injury causes loss of retinal ganglion cells (RGCs) and their axons. The reduction in RGC counts over time in axonal injury is well studied, but the correlation with the timing of anterograde and retrograde axonal degeneration is less clear. The authors longitudinally imaged RGC axons stained with a chloromethyl derivative of fluorescein diacetate (CMFDA) in live rats after optic nerve injury. Methods. Optic nerves were transected. Three days later CMFDA was intravitreously injected. Confocal scanning laser ophthalmoscopy was performed daily, and mean fluorescence intensity and the number of CMFDA bundles were calculated. RGC soma survival was studied after retrograde fluorescence labeling. Retinal nerve fiber layer (RNFL) thickness was evaluated histologically. Results. CMFDA-positive RGC axon bundles could be imaged in vivo. Axons lost 68% +/- 29% of their fluorescence by 7 days after transection compared with 25% +/- 21% in nontransected eyes. The number of labeled axon bundles decreased by 61% +/- 28% at 7 days after transection compared with 26% +/- 9% in nontransected eyes. The number of retrograde-labeled RGCs detected in vivo declined by 53% at 7 days and by 76% at 14 days after transection. RGC soma and CMFDA axon counts decreased most rapidly between 5 and 7 days after transection. Histologic examination demonstrated a reduction in RNFL thickness 7 days after transection. Conclusions. Intravitreal CMFDA can be used to longitudinally monitor RGC axons within the RNFL in vivo. Imaging the disappearance of retrograde-labeled RGC somas and axons indicates that axonal and somal degeneration occur in parallel after axotomy.

Time-course of the retinal nerve fibre layer degeneration after complete intra-orbital optic nerve transection or crush: A comparative study

We examined qualitatively and quantitatively in adult rat retinas the temporal degeneration of the nerve fibre layer after intra-orbital optic nerve transection (IONT) or crush (IONC). Retinal ganglion cell (RGC) axons were identified by their heavy neurofilament subunit phosphorylated isoform (pNFH) expression. Optic nerve injury induces a progressive axonal degeneration which after IONT proceeds mainly with abnormal pNFH-accumulations in RCG axons and after IONC in RGCs somas and dendrites. Importantly, this aberrant pNFH-expression pattern starts earlier and is more dramatic after IONT than after IONC, highlighting the importance that the type of injury has on the time-course of RGC degeneration.

Early cellular signaling responses to axonal injury

BackgroundWe have used optic nerve injury as a model to study early signaling events in neuronal tissue following axonal injury. Optic nerve injury results in the selective death of retinal ganglion cells (RGCs). The time course of cell death takes place over a period of days with the earliest detection of RGC death at about 48 hr post injury. We hypothesized that in the period immediately following axonal injury, there are changes in the soma that signal surrounding glia and neurons and that start programmed cell death. In the current study, we investigated early changes in cellular signaling and gene expression that occur within the first 6 hrs post optic nerve injury.ResultsWe found evidence of cell to cell signaling within 30 min of axonal injury. We detected differences in phosphoproteins and gene expression within the 6 hrs time period. Activation of TNFα and glutamate receptors, two pathways that can initiate cell death, begins in RGCs within 6 hrs following axonal injury. Differential gene expression at 6 hrs post injury included genes involved in cytokine, neurotrophic factor signaling (Socs3) and apoptosis (Bax).ConclusionWe interpret our studies to indicate that both neurons and glia in the retina have been signaled within 30 min after optic nerve injury. The signals are probably initiated by the RGC soma. In addition, signals activating cellular death pathways occur within 6 hrs of injury, which likely lead to RGC degeneration.

Dendritic and Synaptic Protection: Is It Enough to Save the Retinal Ganglion Cell Body and Axon?

Glaucoma and other optic neuropathies have been traditionally viewed as diseases of the optic nerve that lead to retinal ganglion cell (RGC) degeneration. Accordingly, the primary aim of neuroprotective strategies has been to preserve RGC axons and soma. RGCs are complex and highly polarized central neurons, and their pathologic response in disease is likely to be an integration of signals from all cellular compartments-axons, soma, dendrites, and synaptic contacts. We focus on the role of dendrites and dendritic spines in normal neuronal function, neurologic disorders, and glaucoma. The need to understand the mechanisms underlying RGC dendrite and synapse degeneration in glaucoma and other optic neuropathies is compelling, as it may provide insight into novel therapeutic strategies to prevent vision loss.

Regenerating optic axons restore topography after incomplete optic nerve injury

Following complete optic nerve injury in a lizard, Ctenophorus ornatus, retinal ganglion cell (RGC) axons regenerate but fail to restore retinotectal topography unless animals are trained on a visual task (Beazley et al. [ 1997] J Comp Neurol 370:105-120, [2003] J Neurotrauma 20:1263-1270). Here we show that incomplete injury, which leaves some RGC axons intact, restores normal topography. Strict RGC axon topography allowed us to preserve RGC axons on one side of the nerve (projecting to medial tectum) while lesioning those on the other side (projecting to lateral tectum). Topography and response properties for both RGC axon populations were assessed electrophysiologically. The majority of intact RGC axons retained appropriate topography in medial tectum and had normal, consistently brisk, reliable responses. Regenerate RGC axons fell into two classes: those that projected topographically to lateral tectum with responses that tended to habituate and those that lacked topography, responded weakly, and habituated rapidly. Axon tracing by localized retinal application of carbocyanine dyes supported the electrophysiological data. RGC soma counts were normal in both intact and axotomized RGC populations, contrasting with the 30% RGC loss after complete injury. Unlike incomplete optic nerve injury in mammals, where RGC axon regeneration fails and secondary cell death removes many intact RGC somata, lizards experience a "win-win" situation: intact RGC axons favorably influence the functional outcome for regenerating ones and RGCs do not succumb to either primary or secondary cell death.

Anterograde axonal transport of chicken cellular prion protein (PrPc) in vivo requires its N‐terminal part

The cellular isoform of prion protein (PrP(c)) can exist in membrane-bound and secreted forms. Both forms of PrP(c) can be transported by retinal ganglion cell (RGC) axons along the optic nerve in the anterograde direction. In this study we determined which part of chicken PrP(c) is required for its anterograde axonal transport within the optic nerve of embryonic chicken. We intraocularly injected radio-iodinated fragments of recombinant chicken PrP(c) and then examined their anterograde axonal transport from retina into optic tectum. Using gamma-counting and different autoradiographic techniques we quantified anterograde axonal transport of the N-terminal part of chicken PrP(c) (amino acid residues 1-116) in this model system. The transport of the N-terminal part has similar properties as the anterograde transport of full-length chicken PrP(c) (Butowt et al., 2006) described previously (e.g., has similar efficiency, is microtubule-dependent, and is saturable). Moreover, the pattern of ultrastructural distribution of the N-terminal fragment within RGCs is similar to the distribution of full-length PrP(c). The C-terminal fragment of chicken PrP(c) (residues 118-246) and different PrP-derived peptides were not transported. Moreover, PrP(c)-derived peptides were sorted into different endocytotic pathways in neurons, indicating that they cannot substitute for full-length PrP(c) to study its internalization and trafficking. These data indicate that the N-terminal half of chicken PrP(c) contains the necessary information to drive the internalization and subsequent sorting of extracellular PrP(c) in RGCs soma into the anterograde axonal transport pathway.

Three experimental glaucoma models in rats: Comparison of the effects of intraocular pressure elevation on retinal ganglion cell size and death

Glaucoma is a chronic and progressive optic nerve neuropathy involving the death of retinal ganglion cells (RGCs). Elevated intraocular pressure (IOP) is considered to be the major risk factor associated with the development of this neuropathy. The objective of the present study was to compare the effects on RGC survival of three different experimental methods to induce chronic elevation of IOP in rats. These methods were: (i) injections of latex microspheres into the eye anterior chamber; (ii) injections into the anterior chamber of a mixture of microspheres plus hydroxypropylmethylcellulose (HPM) and (iii) cauterization of three episcleral veins. The IOP of right (control) and left (glaucomatous) eyes was measured with an applanation tonometer in awake animals. Thirteen to 30 weeks later, RGCs were retrogradely labeled with 3% fluorogold. Subsequently, we analyzed the density of RGCs, as well as the major axis length and area of RGC soma resulting from the application of each method. A significant increase in IOP was found following application of each of the three methods. Cell death was evident in the glaucomatous eyes as compared to controls. However, no statistical differences were found between the extent of cell death associated with each of the three methods. IOP increase also induced a significant increase in the size of the soma of the remaining RGCs. In conclusion, the three methods used to increase IOP induce a similar degree of RGC death. Moreover, the extent of cell death was similar when the retinas were maintained under conditions of elevated IOP for 24 weeks in comparison to 13 weeks.

Dendritic Abnormalities in Retinal Ganglion Cells of Three-Month Diabetic Rats

Purpose: To determine the effect of three-month diabetes on the retinal ganglion cell (RGC) morphology and density. Methods: Experimental diabetes was induced in Sprague-Dawley rats by intraperitoneal injection of streptozotocin (STZ). Retinas from three-month diabetic and age-matched control rats were harvested, and immunohistochemistry with monoclonal anti-Thy-1 antibody was carried out for calculating RGC density. Random RGC labeling with gene gun propelled lipophilic fluorescent dye, DiI, coated particles (DiOlistic method) was done for detailed RGC classification, dendritic field, and soma size measurement. Results: The number of Thy1-labeled RGCs in the three-month diabetic rats was significantly reduced compared with that in the age-matched control. Obvious RGC morphology changes were observed, and the number of RGCs that could not be classified was significantly greater in the diabetic retinas. Among those well-classified RGCs, cells with enlarged dendritic fields were more frequently seen in the RGA group (401±86um, n = 59, P < 0.001), but the soma sizes were unchanged from the controls (P > 0.05). For cells in the groups of RGB and RGC, no significant changes in the dendritic fields and soma sizes were found (P > 0.05). Conclusions: In the three-month STZ-induced diabetic rat, retinal ganglion cell loss is associated with morphology change. The surviving RGCs in the diabetic retina, especially those in RGA group, show significant dendritic field enlargement. This plasticity of the surviving RGC dendrites may represent a compensatory response to the overall loss of RGCs in diabetes.

A Role for Retinal Brain-Derived Neurotrophic Factor in Ocular Dominance Plasticity

Visual deprivation is a classical tool to study the plasticity of visual cortical connections. After eyelid closure in young animals (monocular deprivation, MD), visual cortical neurons become dominated by the open eye, a phenomenon known as ocular dominance (OD) plasticity . It is commonly held that the molecular mediators of OD plasticity are cortically derived and that the retina is immune to the effects of MD . Recently, it has been reported that visual deprivation induces neurochemical, structural, and functional changes in the retina , but whether these retinal changes contribute to the effects of MD in the cortex is unknown. Here, we provide evidence that brain-derived neurotrophic factor (BDNF) produced in the retina influences OD plasticity. We found a reduction of BDNF expression in the deprived retina of young rats. We compensated this BDNF imbalance between the two eyes by either injecting exogenous BDNF in the deprived eye or reducing endogenous BDNF expression in the nondeprived eye. Both treatments were effective in counteracting the OD shift induced by MD. Retinal BDNF could also influence OD distribution in normal animals. These results show for the first time that OD plasticity is modulated by BDNF produced in the retina.

Anterograde axonal transport of the exogenous cellular isoform of prion protein in the chick visual system

The cellular isoform of endogenous, newly synthesized prion protein (PrP c) can be transported by axons in the anterograde direction. To determine whether a mechanism exists for secreted PrP c to be internalized and then axonally transported, we analyzed internalization and anterograde axonal transport of radiolabeled recombinant PrP c after its intraocular injection in chick embryos. Internalization and axonal transport of exogenous PrP c to the midbrain by retinal ganglion cells (RGCs) is efficient, saturable and likely receptor-mediated. Ultrastructural quantitative localization of radiolabeled PrP c within RGC soma showed significant labeling of vesicular/endosomal compartments and much less labeling present over the Golgi apparatus and lysosomes, which indicates slow degradation of exogenous PrP c in this system. These data show that a mechanism exists to internalize a secreted form of PrP c and then to axonally transport such PrP c in an anterograde direction. This may provide an additional, novel mechanism for prion protein to spread among neurons.

Partial regeneration and long-term survival of rat retinal ganglion cells after optic nerve crush is accompanied by altered expression, phosphorylation and distribution of cytoskeletal proteins.

In a screen to identify genes that are expressed differentially in the retina after partial optic nerve crush, we identified MAP1B as an up-regulated transcript. Western blot analysis of inner retina protein preparations confirmed changes in the protein composition of the microtubule-associated cytoskeleton of crushed vs. uncrushed nerve. MAP1B immunoreactivity and transcript levels were elevated for two weeks after crush. Immunostaining and Western blots with monoclonal antibodies directed against developmentally regulated phosphorylation sites on MAP1B revealed a gradient of MAP1B phosphorylation from the proximal optic nerve stump to the soma of retinal ganglion cells. Most interestingly, using antibodies directed against developmentally regulated phosphorylation sites on MAP1B, we observed that a significant number of crushed optic nerve axons develop MAP1B-immunopositive growth cones, which cross the crush site and migrate along the distal nerve fragment. In parallel, an abnormal distribution of highly phosphorylated neurofilament protein (pNF-H) in the cell soma and dendrites of presumably axotomized retinal ganglion cells was observed following partial nerve crush. This redistribution is present for the period between day 7 and 28 postcrush and is not seen in cells that stay connected to the superior colliculus. Axotomized ganglion cells, which contain pNF-H in soma and dendrites appear to have been disconnected from the colliculus at an early stage but survive axonal trauma for long periods.

Migration of phagocytotic cells and development of the murine intraretinal microglial network: an in vivo study using fluorescent dyes.

This work was undertaken to study whether retinal ganglion cell (RGC) death, which occurs during postnatal development of the mouse retina could aid in assessing the topological and chronological pattern of microglial cell migration. The study was conducted from postnatal day 0 (P0) to adulthood. The fluorescent dyes Fluorogold (FG) or (4-[4-didecylaminostyryl]-N-methylpyridinium iodide (4Di-10ASP) used in this study, were transported retrogradely to the RGC soma when either dye was injected into the superior colliculus (SC) at P0. Some of these labeled RGCs die due to natural apoptosis during this stage of development and are phagocytosed by microglial cells, which move to the site of RGC death, to become labeled with the same dye. The retinas were examined to quantify the microglial cells from P5 to adulthood. In addition, the reaction of microglia to optic nerve crush was studied in adult animals. Both dyes labeled RGCs in the contralateral retina and a few RGCs in the retina ipsilateral to the injected SC. The density of labeled RGCs decreased by 22% between P5 and P7. During this phase, microglial cells become visible as they ingested the fluorescent detritus of the dying RGCs. Microglial cells were evenly distributed across the entire retinal surface and migrated to the outer plexiform layer. Migrating microglia consecutively altered their morphology from the amoeboid to the ramified form. In terms of intracellular storage of the dyes, resident microglial cells retained the fluorescent dye 4Di-10ASP over a period of 12 months. In contrast, FG was completely transferred from the RGCs and microglial cells to intramural cells (pericytes) of the retinal capillaries after 10 months. This resulted in delineation of the entire intraretinal vascular network. Finally, resident retinal microglial cells were also activated by injury to the adult optic nerve and phagocytosed degenerating neurons. Retinal microglial cells can be monitored with vital fluorescent dyes while they migrate across the retina and establish their intra-retinal network. It is possible to label microglia with lipophilic dyes and they remain labeled for a long time. In addition, intramural pericytes can be labeled by slow release of FG from RGCs and microglial cells. The findings suggest that ingested fluorescent dyes having different properties can be used to study different populations of retinal cells in vivo.

Retinal ganglion cells in normal hamsters and hamsters with novel retinal projections. I. Number, distribution, and size

We examined the number, spatial distribution, and size of ganglion cells in the retinae of normal Syrian hamsters and hamsters with retinal projections to the auditory and somatosensory nuclei of the thalamus, induced by neonatal surgery. As revealed by retrograde filling with horseradish peroxidase, there are about 64,600 contralaterally projecting retinal ganglion cells (RGCs) and 1,700 ipsilaterally projecting RGCs in the retinae of normal adult hamsters. Contralaterally projecting RGCs are distributed throughout the retina and have two local density peaks located within a central streak of high RGC density that is oriented approximately along the nasal-temporal axis. RGC density falls above and below the central streak, with a steeper gradient towards the upper retina. Ipsilaterally projecting RGCs are diffusely distributed within a crescent at the inferotemporal retinal periphery and are most dense at the internal border of the crescent. The soma diameter of contralaterally projecting RGCs ranges from 6 to 25 microns; the diameter distribution is unimodal, with a peak in the 10-13 microns range and is skewed toward smaller values, with an elongated tail towards higher values. Contralaterally projecting RGCs tend to be smaller in regions of higher density. Ipsilaterally projecting RGCs tend to be larger than contralaterally projecting RGCs both globally and within the temporal crescent, and their size distributions tend to be less regular and less well related to local density. The retinae of neonatally operated hamsters with novel retinal projections to the auditory. and somatosensory systems contain about one-fourth the normal number of contralaterally projecting RGCs, whose relative density distribution is approximately normal despite the drastic reduction of absolute RGC density. The range and distribution of RGC soma diameters are similar in normal and neonatally operated hamsters, and, in operated as in normal hamsters, contralaterally projecting RGC somata tend to be smaller in regions of higher density. Our results in normal hamsters suggest a role for intraretinal mechanisms in the determination of RGC size. Our findings in neonatally operated hamsters suggest that, despite the reduced number of RGCs in these animals, the same types of RGCs are found in the retinae of normal and neonatally operated hamsters.

A qualitative and quantitative analysis of the response of the retinal ganglion cell soma after stretch injury to the adult guinea-pig optic nerve

The development of a model for focal axonal injury in the optic nerve of the adult guinea-pig has allowed a qualitative and quantitative analysis of the response of the retinal ganglion cell soma to this type of injury. Large and medium sized retinal ganglion cells show classic 'central chromatolysis' in about 30% of ganglion cells between three and seven days after injury, a high proportion of which undergo degeneration between seven and 14 days. Small ganglion cells and small neurons do not demonstrate any morphological response to stretch injury of the optic nerve. However, a small number of larger ganglion cells demonstrate enlargement of the cell soma and nucleolus together with reconstitution of the rough endoplasmic reticulum between seven and 14 days after stretch injury. We suggest that these cells are either recovering from or regenerating after a non-disruptive lesion to their axons. We suggest that some of these morphological changes parallel documented regenerative responses in peripheral/extrinsic neurons after injury to their axons. We conclude that the time course of the 'axon reaction' after stretch injury to axons is longer than that obtained after crush or transection. We provide good morphological evidence that the level of injury after application of non-disruptive mechanical strain to axons is less severe than in the former two models of axonal injury and that a proportion of damaged neurons do not die but rather demonstrate either/or recovery or a regenerative response.

A distinct type of displaced ganglion cell in a mammalian retina

The morphology, dendritic stratification and laminal position of the soma of retinal ganglion cells were analyzed in Golgi preparations and in other rabbit retinas containing cells backfilled from the superior colliculus. Only one type, among 40 Golgi-impregnated types identified, always had its cell body displaced to the amacrine ell sublayer of the inner nuclear layer. The displaced ganglion cell of rabbit retina has a small cell body, very wide dendritic field with sometimes unbranched dendrites extending up to a millimeter from the cell body. The dendritic tree is narrowly stratified just under the amacrine cell bodies in stratum 1, and therefore does not co-stratify with starburst (cholinergic) amacrine cells, but rather with dopaminergic amacrine cells. Its correlate among ganglion cells backfilled from tectum is apparently a very sparse population of small-bodied cells mixed with a variable population of misplaced ganglion cells of varying size and type. The authentic displaced ganglion cell of rabbit retina, unlike the large displaced ganglion cell of birds, is apparently not a directionally selective ganglion cell, and its functional role in vision is presently unknown.

Axonal Transport and Central Visual Projections of Ganglion Cells in Congenitally Blind Chickens

The rd (retinal degenerate) strain of chicken is an example of a recessively inherited mutation characterized by blindness at the time of hatching, as defined by behavioral and electrophysiological tests. Paradoxically, blind mutants have normal retinal morphology, even at the ultrastructural level. Eventually, however, the entire retina degenerates in this strain, perhaps as a result of disuse atrophy. Results of preliminary studies imply that a defect in the visual transduction cascade in photoreceptor cells is responsible for the lack of vision. As well as being an important animal model for studies on photochemistry and transduction, the rd chicken may afford a paradigm for studies on inner retinal physiology and pathology, as electrical input to this inner neuronal system appears to be absent. In the current study we examined axonal transport (both retrograde and anterograde) in rd retinal ganglion cells and connectivity of ganglion cells to visual centers in the brain and compared these to normally sighted chicks. All visuorecipient nuclei were present in rd animals and appeared normal at the light microscopic level. When 3H-proline was injected into one eye of a blind chicken on the day of hatching, labeled polypeptides or proteins were transported via a fast transport mechanism to the same visual centers in roughly the same quantities as in normally sighted chicks. When horseradish peroxidase (HRP) was injected in the optic tectum of blind and normal 1 day old chicks, this label was transported retrogradely to the soma of retinal ganglion cells.(ABSTRACT TRUNCATED AT 250 WORDS)

W-cells in the cat retina: correlated morphological and physiological evidence for two distinct classes.

Intracellular recording and iontophoresis of horseradish peroxidase were used to study the morphology of physiologically characterized W-cells in the cat retina. The recording experiments were performed in an in vivo preparation to allow the responses of these retinal ganglion cells to be compared with previous functional studies of these neurons. The physiological and morphological characteristics of 16 injected and recovered retinal W-cells were compared with similar data from 14 retinal X-cells injected in the same preparations. The soma sizes of retinal W-cells were found to fall into two distinct groups. The somata of the phasic W-cells, at every eccentricity, were smaller than the somata of tonic W-cells, with no overlap between the two distributions. Soma sizes of the tonic W-cells fell into the previously described "medium-sized" range of retinal ganglion cell soma sizes and were similar to, although slightly larger than, the soma sizes of physiologically identified beta- or X-cells. The dendritic arbors of all of the cells physiologically classified as tonic W-cells were similar. Every example of this type had four to five primary dendrites that branched a short distance from the soma to form a circular or cruciate dendritic arbor. The dendritic arrays of these cells were easily distinguishable from the compact dendritic arbors of the physiologically identified X-cells. The dendritic arbors of the phasic W-cells were much more heterogeneous, ranging from sparse, wide dendritic arbors to very compact dendritic arbors with many fine branches. No significant correlation was found between the extent of the dendritic arbor and the distance from the area centralis for either the tonic W-cells or the phasic W-cells. The axons of the tonic and phasic W-cells differed from one another and from X-cells on a number of different morphological and physiological measures. The intraretinal segments of the axons of the phasic W-cells had the smallest diameters of the three groups; the axons of X-cells in the retina were relatively large, and the axons of the tonic W-cells had diameters intermediate between the phasic W-cells and the X-cells. Although considerable overlap was seen between the X-cells, tonic W-cells, and phasic W-cells in their antidromic latencies to electrical stimulation of the optic chiasm, the intraretinal and extraretinal components of the conduction velocities of the three groups were significantly different.(ABSTRACT TRUNCATED AT 400 WORDS)

Loss of retinal X-cells in cats with neonatal or adult visual cortex damage.

Recordings were made from single retinal ganglion cell somas in cats whose visual cortical areas 17 and 18 were damaged on the day of birth or in adulthood. Neonatal lesions produced a 78 percent loss of X-cells in the retina, while lesions made in adulthood produced a 22 percent loss. Y-cells and W-cells were unaffected. This retinal abnormality needs to be considered when interpreting studies of behavioral deficits and neural mechanisms of recovery after damage to the visual cortex.

The ganglíosides of the chicken retina and optic tectum. The influence of light on their labelling after an injection of labelled precursors

Cultures of retinas from 8-day-old embryonic chicken in the presence of (3)H -glucosamine showed that GD3 and GM3 are the gangliosides with highest labelling. From this age onward, and apparently responding to the appearance of the required enzymes, the labelling of GM1, GD1a and GT increases and at hatching day GD1a becomes the highest labelled ganglioside. The main site of synthesis of neuronal gangliosides was found in the neuronal perikarya, in a Golgi membrane enriched fraction. In this fraction the nascent gangliosides are protected from the neuraminidase attack. Experiments in the visual system of chicks indicated that the gangliosides synthesized in the soma of retinal ganglion cells are transported axonally to their endings in the contralateral optic tectum. After 3, 5 and 8 h of injection of N (3)H acetylmannosamine into one eye of the chick, the gangliosides in the contralateral optic tectum of animals exposed to 1000 lux were more labelled than in their controls in dark. The glycoproteins followed a pattern of labelling similar to that of gangliosides. Most of the difference in labelling appears in the same subcellular fraction in which normally is found the maximal deposition of gangliosides. The increase of labelling was not due to a greater turnover of gangliosides.