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PubMed1985

Morphology, central projections, and dendritic field orientation of retinal ganglion cells in the ferret.

Retinal ganglion cells were studied in pigmented ferrets that received small electrophoretic injections of horseradish peroxidase (HRP) into the dorsal lateral geniculate nucleus (LGNd) or optic tract. Ferret retina contains a number of types of retinal ganglion cells of which the relative cell body sizes, dendritic field structures, and central projections correspond closely to those of retinal ganglion cell types in the cat. Ferret retina contains about the same proportion of alphalike cells, a lower proportion of betalike cells, and thus a high proportion of other types of ganglion cells than cat retina. Ferret retina has a visual streak and somewhat weaker area centralis than cat retina. Changes in ganglion cell morphology associated with eccentricity are less pronounced in the ferret than in the cat. The adult ferret retina is about 12.5 mm in diameter, and the nasotemporal division is about 2.7 mm from the temporal margin. Interestingly, virtually all alpha cells in the pigmented ferrets studied projected contralaterally. Studies of infant ferrets indicate that 4 days after birth (P4) the area of ferret retina is 25% that of the adult. The neonatal ferret retina contains numerous small, densely packed cells in the presumptive ganglion cell layer. At P4 these cells appear to be uniformly distributed across the retina. The area centralis and visual streak are not obvious as late as 8 days after birth.

Animals↗
PubMed1986

Cell generation, death, and retinal growth in the development of the hamster retinal ganglion cell layer.

During the early postnatal period in the hamster, the retinal ganglion cell layer grows, establishes its central connections, and undergoes substantial cell loss. In this study, we describe the development of the retinal ganglion cell layer with particular attention to the creation of local specializations in cell density. Changes in the number and spatial distribution of cells identified by a single 3H thymidine injection were examined through the period of maximal cell loss (postnatal days 4-10) and at adulthood. The cells of the retinal ganglion cell layer are generated from embryonic day 10 to postnatal day 3. Overall, cell number in the ganglion cell layer increases by approximately 108,000 cells (223%) from postnatal day 1 to 5, because of continued migration of cells generated prenatally. Cell number decreases from postnatal day 5 to 10 (25%), coincident with the presence of degenerating cells. Cell type is correlated with day of generation: the largest cells, all having retinal ganglion cell morphology, are generated on embryonic days 10 and 11; intermediate-sized cells predominantly of ganglion cell morphology on embryonic day 12; and smaller cells of displaced amacrine or glial cell morphology thereafter. At adulthood, the hamster retina shows a streaklike elevation of cell density through central retina. However, at the time of maximal cell number (postnatal day 5), cell density is uniform across the retina. During the period of cell degeneration, cells are lost in greater relative numbers from the retinal periphery. This cell loss occurs principally from the first-generated cells (embryonic days 10 and 11), as shown by both changes in the distribution of labeled cells and by the spatial pattern of labeled degenerating cells. From postnatal day 10 to adulthood, relative cell density continues to decline in the periphery of the retina, thus suggesting that differential growth completes the production of the adult cell density distribution.

Animals↗
PubMed1986

Morphology of rabbit retinal ganglion cells projecting to the medial terminal nucleus of the accessory optic system.

Rabbit retinal ganglion cells were retrogradely labeled following injection of rhodamine-labeled microspheres into the medial terminal nucleus. The small fraction of rhodamine-labeled neurons reached their peak concentration within the visual streak and then decreased with increasing eccentricity until none were encountered in the far periphery. The same rabbits also received injections of the fluorescent tracer Fast Blue into the superior colliculus. No double-labeled neurons were observed, i.e., ganglion cells projecting to the medial terminal nucleus (MTN) had no axon collaterals to the superior colliculus. In fixed retinae rhodamine-labeled ganglion cells were intracellularly injected with the fluorescent dye Lucifer Yellow to reveal their full dendritic arborization. MTN-projecting cells had medium-sized to large somata with thin and frequently branched dendrites. The large dendritic trees had a distinct morphology and were predominantly unistratified in a narrow band that presumably corresponded to the electrophysiologically determined on-sublamina of the inner plexiform layer. Dendritic field sizes were inversely related to ganglion cell density, thus providing an eccentricity-independent, constant dendritic coverage factor. Approximately five to six dendritic fields from neighboring cells cover every point of the retina. Published reports claim that the physiological class of on-direction-selective ganglion cells provides the sole retinal input to the MTN in the rabbit. In this context morphological features of MTN-projecting cells and their presumed functional correlation with on-direction-selective ganglion cells are discussed.

Animals↗
PubMed1989

Prevention of optic nerve regeneration in the frog Hyla moorei transiently delays the death of some ganglion cells.

We have previously reported that a proportion of ganglion cells die during optic nerve regeneration in the adult frog Hyla moorei (Humphrey and Beazley, '85). Here we assess the effect of preventing optic nerve regeneration on this cell loss. The optic nerve was crushed unilaterally and regeneration was allowed to progress unimpeded in one experimental series but was prevented by ligating or capping the nerve in another. We estimated total cell numbers in the ganglion cell layer from cresyl-stained wholemounts, comparing each experimental retina with its unoperated partner. At 70-78 days postcrush, mean cell numbers had fallen by 31.5% for frogs with unimpeded regeneration (N = 9), a significantly greater reduction than the 21.5% (N = 8) loss for the impeded regeneration series (p less than 0.001). Thereafter, cell numbers were stable for frogs with unimpeded regeneration. Cell death continued in the series with impeded regeneration, and losses exceeded those of frogs with unimpeded regeneration from 110 days postcrush. When regeneration was impeded, ganglion cell somas underwent an intense cell soma reaction and became arranged in rows radiating from the optic nerve head. Our findings indicate that some ganglion cells are transiently spared when regeneration of their axons is prevented. The abnormally extensive contacts formed between somas may delay ganglion cell loss. However, the eventual death of most ganglion cells shows them to be target-independent in the long term.

Animals↗
PubMed1990

Dendritic morphologies of retinal ganglion cells projecting to the lateral geniculate nucleus in the rabbit.

Small injections of fluorescent Rhodamine-latex microspheres and Fast Blue were made into the dorsal lateral geniculate nucleus (dLGN) of fifteen rabbits. After 8-15 day survival times, the somas of projecting ganglion cells were found to be labelled in the contralateral retinas by retrograde transport. The dendritic morphologies of the labelled ganglion cells were revealed by intracellular injection of Lucifer Yellow or horseradish peroxidase while superfusing the retinas. At least ten distinct dendritic morphologies were observed among 161 injected ganglion cells. The three most commonly recovered dendritic morphologies were those of: (1) alpha-like cells; (2) large, complex dendritic field cells; and (3) cells with small, dense dendritic fields that resemble intracellularly identified brisk sustained cells (Amthor et al., J. Comp. Neurol. 1989; 280:72-96). Smaller percentages of cells whose dendritic morphologies resembled those of several physiologically identified sluggish and complex receptive field ganglion cell classes (Amthor et al., J. Comp. Neurol. 1989; 280:72-96, 97-21) were also recovered. Several morphological types were also found that were previously unknown or could not be confidently related to those of previously known classes. Most dLGN injections labelled many different types of ganglion cells, but restricted injections in some dLGN loci labelled only a limited number of ganglion cell classes.

Animals↗
PubMed1992

Independent mosaics of large inner- and outer-stratified ganglion cells in the goldfish retina.

Goldfish retinal ganglion cells were filled with horseradish peroxidase and studied in flatmounts. Two regular mosaics of large neurons with many of the properties of mammalian alpha ganglion cells were found, differing from each other in spacing, size, and dendritic stratification. The existence of biplexiform ganglion cells with additional dendrites in the outer plexiform layer was also confirmed. One of the two alpha-like mosaics consisted of giant ganglion cells with thick primary dendrites and large, sparsely branched dendritic trees in the outer sublamina of the inner plexiform layer (IPL). In fish 55-65 mm long, about 300 formed a tessellated array across each retina. Their somata (mean area 277 +/- 6 microns 2) were displaced to varying degrees into the IPL, neighbours in the mosaic often occupying different levels. Their dendrites ramified in one stratum near the inner nuclear layer, at a mean depth of 70.8 +/- 0.5% of the IPL. The other alpha-like mosaic comprised about 900 large ganglion cells, with slightly smaller somata (mean area 193 +/- 4 microns 2) in the ganglion cell layer. Most of their dendrites lay in a narrow stratum at 41.9 +/- 0.5% of the depth of the IPL. However, deviations (usually into more vitread strata) were common, which was not true for similar cells in the distantly related cichlid fish Oreochromis. Measurements of nearest neighbour distance (NND) for 4 outer and 4 inner mosaics showed that they were at least as regular as the alpha cell mosaics of mammals: the ratio of the mean NND to the standard deviation ranged from 4.03 for the least regular outer mosaic to 6.47 for the most regular inner mosaic. The wide phylogenetic distribution of these paired, regular mosaics points to a fundamental role in vision. The presence of some variability in dendritic stratification even within the exceptionally regular inner-stratified mosaic suggests that classifications based entirely on the detailed morphology of individual neurons may not always correlate well with their primary functional roles. Where possible, neuronal morphology and spatial distribution should be studied together.

Animals↗
PubMed1992

Genesis of neurons in the retinal ganglion cell layer of the monkey.

We have analyzed the genesis of various neuronal classes and subclasses in the ganglion cell layer of the primate retina. Neurons were classified according to their size and the time of their origin was determined by pulse labeling with 3H-thymidine administered to female monkeys 38 to 70 days pregnant. All offspring were sacrificed postnatally, and their retinas processed for autoradiography. The somata of cells in the retinal ganglion cell layer generated on embryonic day (E) 38 ranged from 9 to 14 microns in diameter. Between E40 and E56, the minimum soma diameter remained around 8-9 microns, while the maximum gradually increased to 22 microns. As a consequence, the means of the distributions of labeled cells also increased with age, from 11.8 microns diameter for cells generated on E38 to 14.6 microns diameter at E56. Over this period the percentage of labeled cells in the 10.5-16.5 microns and greater than 16.5 microns diameter range gradually increased. The proportion of the labeled cells in the less than 10.5 microns diameter range decreased from E38 to E45, but subsequently increased rapidly. At the end of neurogenesis in the retinal ganglion cell layer, around E70, most labeled cells were considerably smaller (7-9 microns) than those generated earlier. Our results indicate that within the ganglion cell layer of the macaque, neurons of small caliber are generated first, followed successively by medium sized cells. Large, putative P alpha cells are generated late. The production between E56 and E70 of cells with the smallest somata suggests that the last-generated neurons in the ganglion cell layer are predominantly displaced amacrine cells. Within the same sector of retina, different classes of neurons in the ganglion cell layer of the rhesus monkey appear to have a sequential schedule of production.

Animals↗
PubMed1992

Lucifer yellow, retrograde tracers, and fractal analysis characterise adult ferret retinal ganglion cells.

The dendritic morphology of retinal ganglion cells in the ferret was studied by the intracellular injection of lucifer yellow in fixed tissue. Ganglion cells were identified by the retrograde transport of red or green fluorescent microspheres that had been injected into different target nuclei, usually the lateral geniculate nucleus or superior colliculus. This approach allows the comparison of dendritic morphologies of ganglion cells in the same retina with different central projections and also identifies cells with branching axons. The digitised images of dendritic arbors were analysed quantitatively by a variety of measures. Dendritic complexity was assessed by calculating the fractal dimension of each arbor. The ferret has distinct alpha, beta, and gamma morphological classes of cells similar to those found in the cat. The gamma cell class was morphologically diverse and could be subdivided into "sparse," "loose," and "tight" groups, reflecting increasing dendritic complexity. Whereas the beta cell projection was limited to the lateral geniculate nucleus alone, alpha and gamma cells could project to either or both nuclei. Retinal ganglion cells labelled from the pretectal nuclei formed a morphologically distinct class of retinal ganglion cells. The ipsilateral projection lacked alpha cells and the most complex, "tight" gamma cells. However, ipsilaterally projecting "loose" gamma cells overlapped alpha cells in both soma and dendritic dimensions. Different morphological classes of retinal ganglion cells hence show characteristic axon behaviour both in their decussation at the chiasm and in which targets they innervate. Fractal measures were used to contrast variation within and between these identified classes.

Animals↗
PubMed1992

Topography of ganglion cells in the dog and wolf retina.

The topographical distribution of retinal ganglion cells in seven breeds of dog (Canis lupus f. familiaris) and in the wolf (Canis lupus) was studied in retinal wholemounts stained with cresyl violet or with a reduced silver method. A prominent feature of all wolf retinae was a pronounced "visual streak" of high ganglion cell density, extending from the central area far into both temporal and nasal retina. By contrast, either a pronounced or a moderate visual streak was found in dog retinae. It is hypothesized that a pronounced streak is an archetypal feature of Canis lupus, and that the moderate streak in some dogs is a corollary of breeding during domestication. Irrespective of the differences in streak form and retinal area, the estimated total number of ganglion cells was about 200,000 cells in the wolf and 115,000 in the dog. Ganglion cell density maxima in the central area of the wolf were about 12,000-14,000/mm2, and in the dog they ranged from 6,400/mm2 to 14,400/mm2. This implies individual differences in visual acuity. Alpha ganglion cells constituted 3-14% of all ganglion cells in the dog and 1-18% in the wolf, depending on retinal location. A distinct feature of all dogs and wolves was the absence of alpha cells in a substantial region of temporal peripheral retina. This has not been found in any other mammalian species and suggests corresponding functional deficits.

Animals↗
PubMed1993

NGF augmentation rescues trigeminal ganglion and principalis neurons, but not brainstem or cortical whisker patterns, after infraorbital nerve injury at birth.

Prior studies indicate that neonatal nerve injury kills many trigeminal (V) first- and second-order cells, and interrupts pattern formation in the brainstem and cerebral cortex. Yet it is not known whether effects upon cell survival and pattern formation are causally related. To determine whether axotomized V ganglion cells can be rescued by an exogenous trophic agent, rats received 5 mg/kg of nerve growth factor (NGF) prior to, and every day after, infraorbital nerve section on the day of birth until sacrifice on postnatal day (PND) 1, 3, 5, 7, or 14. Other animals received identical lesions without NGF. Ganglion cell numbers were significantly reduced by PND1 in pups not given NGF, while NGF-treated rats displayed no significant cell loss through PND7. However, NGF did not permanently rescue V neurons because ganglion cell numbers were reliably reduced by PND14. Cell numbers in V nucleus principalis were reduced by PND1 in pups not given NGF, while NGF-treated animals displayed no cell loss through PND14. NGF's rescue of second-order cells is probably an indirect effect of NGF action upon V ganglion cells because, in other newborns, NGF failed to maintain principalis cells after direct lesion of the left V ganglion. To determine whether preventing cell death permits whisker-related pattern formation, other rats also received NGF prior to and after infraorbital nerve section at birth. After 3-14 days, patterns were assessed in the brainstem and cortex with cytochrome oxidase histochemistry and serotonin immunocytochemistry. Whisker-related patterns failed to develop as in cases not given NGF. These data indicate that communication with the periphery is necessary for the maintenance of central whisker-related patterns. They also suggest that V ganglion cells can be rescued, albeit temporarily, from rapid injury-induced death by NGF, thereby delaying injury-induced cell death in nucleus principalis. However, the mechanism(s) responsible for injury-induced pattern alterations in the developing V system remains to be elucidated.

Animals↗
PubMed1995

Large retinal ganglion cells in the channel catfish (Ictalurus punctatus): three types with distinct dendritic stratification patterns form similar but independent mosaics.

Retinal ganglion cells in the channel catfish (Ictalurus punctatus) were retrogradely labelled, and those with the largest somata and thickest primary dendrites were categorized by their levels of dendritic stratification. Three types were found, each forming a mosaic making up approximately 1% of the ganglion cell population. Using a system based on established sublaminar terminology, we call these the alpha-a (alpha a), alpha-b (alpha b), and alpha-c (alpha c) ganglion cell mosaics. Cells of the alpha a mosaic had large, sparsely branched trees in sublamina a at 10-30% of the depth of the inner plexiform layer (IPL), sclerad to those of all other large ganglion cells. Some alpha a somata were displaced into the IPL or inner nuclear layer (INL) but belonged to the same mosaic as their orthotopic counterparts. Cells of the alpha b mosaic had dendrites that branched a little more and arborized in sublamina b at 50-60% of the IPL depth. Many also sent fine branches into sublamina a, and some were fully bistratified in a and b. The alpha c cells arborized in the most vitread sublamina, sublamina c, at 80-95% of the IPL depth. The soma areas of the three types in the largest retina studied ranged between 139 microns 2 and 670 microns 2 with significant differences in the order alpha a > alpha c > or = alpha b. Analyses based on nearest-neighbour distance (NND) and on spatial auto- and cross-correlograms showed that each mosaic was statistically regular and independent of the others. Mosaic spacings were similar for each type, giving mean NNDs of 242-279 microns in the largest retina and 153-159 microns in a smaller one. Correspondences between these mosaics, previously defined large ganglion cell types in catfish, and other mosaic-forming large ganglion cells in fish and frogs are discussed along with their implications for neuronal classification, function, development, and evolution.

Animals↗
PubMed1994

A thymidine kinase deficient HSV-2 strain causes acute keratitis and establishes trigeminal ganglionic latency, but poorly reactivates in vivo.

The incidence of herpetic keratitis following intranasal or direct ocular infection with thymidine kinase-negative (TK-) strains of herpes simplex virus (HSV)-2 has not been well studied, and the role of the TK gene in the establishment of latency and virus reactivation is controversial. To determine whether a TK- strain of HSV-2 could establish trigeminal ganglionic latency and be reactivated in vivo to produce recurrent keratitis or nervous system infection, an animal model of acute and recurrent infection was utilized. Rabbits were infected by the intranasal or ocular routes, and latency was reactivated by immunosuppression. Virus shedding in nasal and ocular secretions was monitored, and the eyes were examined for the presence of corneal epithelial lesions during acute and reactivated infections. Central nervous system (CNS) and trigeminal ganglionic tissues were assayed by histologic, virologic, and in situ hybridization techniques. All rabbits intranasally infected shed virus in both ocular and nasal secretions, whereas only 30% of rabbits infected in the eyes shed virus in nasal secretions. Virus was recovered from cocultivation cultures, but not from cell-free homogenates, of trigeminal ganglionic and CNS tissues from animals inoculated by both routes. The incidence of keratitis was much greater after direct ocular inoculation, although both routes of inoculation produced CNS and ganglionic inflammatory lesions. Keratitis healed in 92% of the animals infected by the ocular route by 26 days post infection. Of rabbits initially infected in the eyes and then subjected to drug-induced reactivation, only 30% shed virus, which was limited to a 24 hour period; there was no reappearance of epithelial keratitis, no animal became blind, and none died. In contrast, latently infected control rabbits uniformly reactivated. These studies show that this TK-HSV-2 strain (i) replicates in the eye, (ii) is neuroinvasive but non-neurovirulent following intranasal and direct ocular infection; (iii) sheds in the eye more frequently and for longer periods after ocular than after intranasal inoculation; (iv) induces epithelial keratitis that usually heals spontaneously; (v) establishes latency in trigeminal ganglionic neurons, but no other ganglionic cells; and, (vi) reactivates in a small proportion of animals, but does not produce recurrent ocular lesions following drug-induced immunosuppression. Thus, the TK gene appears directly involved in HSV latency and reactivation in vivo.

Animals↗
PubMed1999

Extrinsic modulation of retinal ganglion cell projections: analysis of the albino mutation in pigmentation mosaic mice.

Tyrosinase is a key enzyme involved in the synthesis of melanin in the retinal pigment epithelium (RPE). Mice that are homozygous for the albino allele at the tyrosinase locus have fewer retinal ganglion cells with uncrossed projections at the optic chiasm. To determine the site of the albino gene action we studied the projections of retinal ganglion cells in two types of pigmentation mosaic mice. First, we generated mosaic mice that contain a translocated allele of the wild-type tyrosinase on one X chromosome but that also have the lacZ reporter transgene on the opposite X chromosome. In these lacZ/tyrosinase mice, which are homozygous for the albino allele on chromosome 7, X-inactivation ensures that tyrosinase cannot be functional within 50% of the retinal ganglion cells and that these individual cells can be identified by their expression of the lacZ reporter gene product, beta-galactosidase. The proportion of uncrossed retinal ganglion cells expressing beta-galactosidase was found to be identical to the proportion that did not express it, indicating that the albino mutation associated with axonal behavior at the optic chiasm must affect ganglion cells in a cell-extrinsic manner. Second, to determine whether the RPE is the source of the extrinsic signal, we generated aggregation chimeras between pigmented and albino mice. In these mosaic mice, the extent of the uncrossed projection corresponded with the amount of pigmented cells within the RPE, but did not correspond with the genotypes of neural retinal cells. These studies demonstrate that the albino mutation acts indirectly upon retinal ganglion cells, which in turn respond by making axonal guidance errors at the optic chiasm.

Albinism↗
PubMed2000

Suppressive actions of betaxolol on ionic currents in retinal ganglion cells may explain its neuroprotective effects.

Betaxolol, a beta 1-selective adrenoceptor antagonist, is widely used in the treatment of glaucoma. In addition to its ocular hypotensive effects, betaxolol has been suggested to act as a retinal neuroprotective agent (Osborne et al., 1997). To investigate possible mechanisms underlying the neuroprotective effects, we tested the actions of betaxolol on ion channels and calcium signaling in isolated retinal ganglion cells. Betaxolol (50 microM) reduced by about 20% the high-voltage-activated (HVA) Ca channel currents in ganglion cells isolated from tiger salamander retina. In contrast, the beta 1-adrenoceptor antagonists propranolol (10 microM) and timolol (50 microM) had no inhibitory actions on HVA Ca channel currents. The L-type Ca channel antagonist, nisoldipine, blocked the HVA Ca channel current partially and the remaining current was not inhibited by betaxolol. Outward current was inhibited in the presence of betaxolol. Both iberiotoxin (IBTX; 10 nM), a selective inhibitor of large-conductance Ca-activated K channels, and Cd2+ (100 microM), which suppresses Ca-activated K channels subsequent to its block of Ca channels, reduced outward current and the remaining current was not blocked significantly with betaxolol. In the presence of betaxolol, Na channel currents were reduced by about 20%, as were currents evoked by glutamate (10 mM) and GABA (1 mM). Current clamp recordings from isolated ganglion cells showed that betaxolol had several effects on excitability: spike height decreased, repetitive spike activity was suppressed, spike width increased and hyperpolarization following spikes was reduced. Calcium imaging in isolated rat retinal ganglion cells revealed that betaxolol inhibited glutamate-induced increases in [Ca2+]i. These results suggest that betaxolol has a diversity of suppressive actions on ganglion cell ion channels and that, as a consequence, one of the net actions of the drug is to reduce Ca2+ influx. The subsequent reduction in [Ca2+]i may contribute to the apparent neuroprotective actions of betaxolol in promoting ganglion cell survival following ischemic insult, as may occur in glaucoma and retinal disease.

Action Potentials↗
PubMed1993

Atrophy and degeneration of ganglion cells in central retina following loss of postsynaptic target neurons in the dorsal lateral geniculate nucleus of the adult cat.

Selective degeneration of neurons in the dorsal lateral geniculate nucleus (dLGN) of the adult cat was produced by in situ injection of kainic acid. This rapid degeneration mimics the loss of lateral geniculate neurons seen after neonatal visual cortex ablation. Following survivals of 2, 4, or 6 months, the geniculate was injected with horseradish peroxidase (HRP) and the retinas were examined for the presence of retrogradely labeled, as well as unlabeled, cells. Total ganglion cell density in central nasal retina was not different from that of controls at 2 or 4 months, but by 6 months had decreased to 68% of control values. The proportion of cells labeled with HRP did not change at 2 months, but decreased from 84% in controls to less than 1% by 4 months, and none were labeled at 6 months. Surviving ganglion cells in central retina showed atrophy of the cell body, a finding not apparent in data from the retinal periphery. Shrinkage occurred in the few cells labeled with HRP surviving at 4 months, as well as among the unlabeled cells surviving at 4 and 6 months. These results show that the survival of central retinal ganglion cells in the cat continues to depend on intact target neurons beyond the period of development. Mature ganglion cells in central retina respond to loss of appropriate targets first by axon terminal retraction and then by atrophy and cell death. However, when compared to the response of cells located in far peripheral retina following dLGN neuron loss, central ganglion cells take longer to undergo axonal retraction and a greater proportion of the central ganglion cells, although atrophied, survive after 6 months.

Analysis of Variance↗
PubMed1993

Tritiated uridine uptake in the retinal ganglion cell layer of the cat during normal development and after visual cortex ablation.

The short-term metabolic response of immature retinal ganglion cells to destruction of their target cells in the dorsal lateral geniculate nucleus (dLGN) was assessed in newborn cats. Retrograde degeneration of virtually all dLGN cells was induced by ablation of the 13 contiguous areas of visual cortex on the day of birth. The metabolic response of retinal ganglion cells to this loss of target cells in dLGN was determined by exposing the ganglion cell layer to tritiated uridine, a precursor of RNA. Control measurements were made from unoperated littermates. Following sectioning and processing of the retinae from both groups of kittens for autoradiography, silver grain densities overlying the cellular profiles in the ganglion cell layer were calculated. These calculations revealed levels of uridine incorporation at Postnatal Day 4 in both groups of kittens significantly higher than at either Postnatal Day 2 or 7, but no significant differences between the two groups on any day examined. These results show that the level of RNA synthesis in retinal ganglion cells increases temporarily during the first postnatal week and that this synthesis is unaffected by the death of target cells in the dLGN. The temporary increase may be related to the establishment of synaptic connections on retinal ganglion cells by their afferent bipolar and amacrine neurons in the inner nuclear layer.

Animals↗
PubMed1988

Alterations in the morphology of ganglion cell dendrites in the adult rat retina after optic nerve transection and grafting of peripheral nerve segments.

Transected ganglion cell axons from the adult retina are capable of reinnervating their central targets by growing into transplanted peripheral nerve (PN) segments. Injury of the optic nerve causes various metabolic and morphological changes in the retinal ganglion cell (RGC) perikarya and in the dendrites. The present work examined the dendritic trees of those ganglion cells surviving axotomy and of those whose served axons re-elongated in PN grafts to reach either the superior colliculus (SC), transplanted SC, or transplanted autologous thigh muscle. The elaboration of the dendritic trees was visualized by means of the strongly fluorescent carbocyanine dye DiI, which is taken up by axons and transported to the cell bodies and from there to the dendritic branches. Alternatively, retinofugal axons regrowing through PN grafts were anterogradely filled from the eye cup with rhodamine B-isothiocyanate. The transection of the optic nerve resulted in characteristic changes in the ganglion cell dendrites, particularly in the degeneration of most of the terminal and preterminal dendritic branches. This occurred within the first 1 to 2 weeks following axotomy. The different types of ganglion cells appear to vary in their sensitivity to axotomy, as reflected by a rapid degeneration of certain cell dendrites after severance of the optic nerve. The most vulnerable cells were those with small perikarya and small dendritic fields (type II), whereas larger cells with larger dendritic fields (type I and III) were slower to respond and less dramatically affected. Regrowth of the lesioned axons in peripheral nerve grafts and reconnection of the retina with various tissues did not result in a significant immediate recovery of ganglion cell dendrites, although it did prevent some axotomized cells from further progression toward posttraumatic cell death.

Animals↗
PubMed1985

Retinal input to the nucleus of the optic tract of the cat assessed by antidromic activation of ganglion cells.

We have studied the physiological properties of ganglion cells in the retina of the cat. The experiments were designed to identify those ganglion cells which project to direction-selective cells in the nucleus of the optic tract (NOT), by demonstrating their antidromic activation at low threshold from an electrode in the NOT. These ganglion cells presumably provide the retinal drive to the optokinetic reflex. Altogether, 11 such ganglion cells were identified in a population of 578 cells studied. All 11 were W-cells, with slow-conducting axons. Five of the 11 had on-centre direction-selective receptive fields; the other 6 had a variety of receptive field patterns. Thus, on centre-selective cells form a much higher proportion of the retinal input to direction-selective cells in the NOT than of the overall ganglion cell population. However, their receptive field properties were too varied fully to account for the selectivity of NOT cells for horizontal stimulus movement. In summary the retinal input to the NOT appears to be formed principally or entirely by W-class ganglion cells, including many which are direction selective. It still seems necessary, however, to postulate, some non-retinal mechanism to account for all the receptive field properties of direction-selective NOT cells.

Afferent Pathways↗